Welcome to the Fate Therapeutics Fourth Quarter 2020 Financial Results Conference Call. At this time, all participants are in a listen-only mode. This call is being webcast live on the Investors and Media section on Fate's Web site at fatetherapeutics.com. As a reminder, today's call is being recorded. I would now like to introduce Scott Wolchko, President and CEO of Fate Therapeutics. The floor is yours.

Thank you. Good afternoon, and thanks everyone for joining us for the Fate Therapeutics fourth quarter 2020 financial results call. Shortly after 4:00 P.M. Eastern Time today, we issued a press release with these results, which can be found on the Investor section of our Web site under Press Releases. In addition, our Form 10-K for the year ended December 31, 2020 was filed shortly thereafter and can be found on the Investor section of our Web site under Financial Information. Before we begin, I'd like to remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward-looking statements. Please see the forward-looking statement disclaimer on the company's earnings press release issued after the close of market today as well as the risk factors in the company's SEC filings included in our Form 10-K for the year ended December 31, 2020 that was filed with the SEC today. Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, Fate Therapeutics disclaims any obligation to update these forward-looking statements to reflect future information, events or circumstances. Joining me on today's call are Dr. Wayne Chu, our Senior Vice President of Clinical development; Ed Dulac, our Chief Financial Officer; Dr. Dan Shoemaker, our Chief Scientific Officer; and Dr. Bob Valamehr, our Chief Development Officer. Today we will review some of the clinical data for FT516 and FT596 programs that we…

Thank you, Scott. Turning to our financial results, revenue was $15.9 million for the fourth quarter of 2020 compared to $2.8 million for the same period last year. Revenue in the current quarter was derived from our collaborations with Janssen and ONO pharmaceutical. In December, we shared with ONO, a preclinical data package for an iPSC derived CAR T cell product candidate incorporating ONOs proprietary antigen binding domain targeting a cancer specific antigen expressed on certain solid tumors. Based on these data ONO elected to continue preclinical development of the product candidate under the collaboration and we received a $10 million milestone fee from ONO. As a reminder, ONO maintains an option to develop and commercialize the iPSC derived CAR T cell product candidate in all territories of the world. And we retain the right to co-develop and co-commercialize the product candidate in United States and Europe under a joint arrangement where we are eligible to share at least 50% of the profits and losses. In the fourth quarter, we recognized $6.1 million of the $10 million milestone payment received from ONO. Research and development expenses for the fourth quarter of 2020 were $39 million compared to $25.2 million for the same period last year. The increase in R&D expenses was attributable primarily to an increase in employee headcount and compensation, including share based compensation and expenses associated with the facility lease for our new corporate headquarters. General and administrative expenses for the fourth quarter of 2020 were $10.3 million compared to $6.7 million for the same period last year. The increase in our G&A expenses was attributable primarily to an increase in headcount and employee compensation, including share based compensation. Total operating expenses for the fourth quarter of 2020 were $40.5 million net of $8.8 million in non-cash share…

Hey guys, this is Kripa for Robyn. Thank you so much for taking my call and congratulations in all the progress. One question I had was in addition to your partnerships that with ONO and Janssen, what is your strategy and bandwidth for any additional potential partnerships? And especially if those that include your wholly-owned products?

Sure, happy to answer that. I think we absolutely have a platform that is amenable and we have bandwidth to do additional partnerships as well as increase the existing partnerships if we chose to do so.

Great. And then, you have you plan to start initiate an AML program with FT538, would you need to see data from the monotherapy trial before you initiate the combo? Or can they be run in parallel? And also, it seems like you're continuing to enroll patients in the FT516 trial for AML, can you maybe talk about your overall strategy in AML?

Sure. So I'll start long-term vision, long-term vision in AML. I think at the end of the day, we're very interested in targeted strategies for AML. Certainly, historically, non-engineered donor derived NK cells have shown activity, I think in about 20% to 25% of patients donor derived NK cells, again, not engineered, not targeted, in any express way, have been able to drive responses. But I do think there's significant room for improvement, just like we've seen in other hematologic malignancies. And so the long-term strategy in AML, I think would be to absolutely have a targeted approach. It was one of the reasons we were really intrigued by the data that we saw at EHA with respect to CD38 expression on leukemic blasts and potentially, which we're now doing combining FT538 with daratumumab in AML, as a first means of looking at a targeted strategy.

Your next question comes from the line of Alethia Young from Cantor.

And certainly it's been an exciting past three or four months. I just wanted to kind of go back to the notion of r dosing and the conditioning regimen review. I've got a couple questions I think recently around how viable it might be to use a conditioning regimen kind of if you had to do it -- you've had to deal with couple of times. And maybe the second part of that question is, are you considering maybe a lighter version of a conditioning regimen? I mean, so far, the profile has seemed pretty benign as far as the drug itself? Thanks.

Wayne and I are not in the same room. Wayne, are you there? You want to address?

That's a great question. Thank you for asking. I think that one of the fundamental questions, for our clinical programs and I don't speak just for the Fate portfolio, but I would say all sponsors are developing the cellular therapies, is really defining the nature of the conditioning regimen. We currently are utilizing the combinations of fludarabine and cyclophosphamide across our trials. I should note that there are some differences with respect to the schedule and the doses that we're using, depending on the indication being tested. So I think one of the things that we're trying to understand, with our current slate of trials, is directly addressing the question you raised around what is the tolerability of a patient to receive potentially multiple rounds of condition that's consistent fludarabine and cyclophosphamide. And I think it's probably worth mentioning the fact that the combination of Flu/Cy does have clinical precedent. For example, in patients who are newly diagnosed with chronic lymphocytic leukemia, one of the more common immuno chemotherapy regimens is the combination of Rituximab with Flu and Cy. And so there is some clinical precedence to the idea of being able to give multiple rounds of Flu/Cy containing regimen. But I think an important question which we plan to address as part of our ongoing studies is to see whether or not things like dose adjustment to the fludarabine and cyclophosphamide dose are feasible, not only from a patient safety and tolerability perspective, but also with respect to their ability to support with pharmacokinetic profile of our product candidates. We are also very interested in understanding whether or not other combinations of therapies can be used as conditioning such that we're not necessarily wed to a paradigm that involves fludarabine and cyclophosphamide conditioning. And those ideas are all being on the table and we hope to include initial clinical experiments to address that question in the not too distant future as part of our current study.

Your next question comes from the line of Michael Schmidt from Guggenheim.

I had two actually, one bigger picture question around pipelines strategy, obviously, your engineered NK cell pipeline is much more expensive than your CAR T program at this point. I was just wondering longer term how you think the Fate portfolio may evolve? And will it be maybe more NK cell-centric as opposed to CAR T focus? So that's my first question. And I have a follow up.

Sure. I can start with that. Obviously, you're well aware of the history of the company. And we certainly got a head start with NK cells as compared to T cells. There's a long history of using IPS cell technology to derive T cells, which quite honestly started with our collaborator, Memorial Sloan Kettering, Michel Sadelain. And initially, he was able to develop gamma delta T cells and published on that, I want to say probably around 2015. Our collaboration with him was expressly around making alpha beta T cells. And we think, we've actually nailed that quite well and are really excited about advancing 819 into clinical development this year. I would sort of underscore, yes, we are absolutely more advanced on NK cells. And we are pushing very hard with respect to the NK cell side of our pipeline and are quite honestly super excited about what we're seeing. But let's also acknowledge that there's been some really exciting results and patient responses that have been generated with T cells. And our collaborations including our ONO collaboration and our Janssen collaboration do involve the development of IPS derived CAR T cell candidates. So I would say that while for instance, our NK cell pipeline is more mature, I would not take that as an indication that we are significantly betting on an NK cell approach over a T cell approach. We're absolutely developing both cell types aggressively.

Great, thanks. And then, a question on 516, specifically, you did mention that you're now planning the first expansion cohort on DLBCL. And I was just wondering around the dosing paradigm, I know you've talked about giving multiple doses over time et cetera. At the same time, you have seen already deep and good responses after only giving one or two cycle and the dose escalation. So I was just wondering how you thinking about the dosing paradigm in this expansion cohort? Will this be a fixed cycle or fixed time duration, dosing paradigm? Or will it be a chronic regimen more akin to an monoclonal antibody therapy?

Yes. So, great question. I think what you will see us do as part of dose expansion is continue with where we have seen success. So we will likely kick off a dose expansion that includes the existing treatment paradigm with FT516. At the same time, you should not be surprised if we also experiment with other treatments cycles with FT516, which may involve for instance, we were just discussing Cy/Flu, it may involve less Cy/Flu, it may involve a conditioning regimen that is not Cy/Flu and it may involve longer duration of dosing of FT516. But there will at least be a core arm of dose expansion that involves the existing treatment paradigm where we are seeing and are excited by the responses.

Next is from Yigal Nochomovitz from Citi.

I had a broad on your myeloma franchise strategy, obviously, there are two programs for myeloma and combo with daratumumab with [indiscernible] FT576. So can you talk about the development strategy there? Are you prepared to advance both combo regimens into later stage trials? Or is your objective to settle on one data combo after you're done with Phase 1?

Yes, it's a great question. I think it's too early for us to say what our long-term strategy is necessarily. I mean, we have to see sort of what the profiles of both product candidates are. Obviously, we are really encouraged by, if you go to the lymphoma side, we're super encouraged what we're seeing with FT516 and we're pushing FT516 aggressively forward even though we have ft 596. And we're excited by FT596, there may be opportunities for both programs in different lines of treatment, absolutely. And I think we're approaching myeloma, from that same perspective, that we're very open minded, we're going to let the data guide us, the clinical data guide us as to the potential for the product candidates. Generally I will still continue to say, I mean, I do think multi-antigen targeting offers best-in-class potential, but obviously that needs to play out in the clinic and there's very few multi-targeted programs in clinical development of any kind whether IPS derived or patient or donor derived. I would say today, I mean, certainly our confidence has been significantly bolstered in our proprietary CD16 receptor and its ability to promote ADCC with monoclonal antibody therapy.

Okay, thanks. And then turning to AML, the EHA data that you mentioned, the 239 and the 241 expressing CD38 is obviously very interesting. Is that a fair assumption, therefore, that for this combo study, that you've announced the 538 cluster, that you're not going to do any screening for CD38? You're just going to take AML patients?

That's correct. We're not screening for CD38 in advance, but obviously, in getting bone marrow biopsies we'll be able to assess for them.

Okay. And then just one question on your preclinical program, on the CAR B7H3, is that the correct expectation that the multiplex engineering is going to include the high affinity non-cleavable, CD16 and the IL-15 receptor fusion? And are there other functionalities beyond those two that you might be developing for this program?

Sure, I'll let Bob answer that question. But before I turn it over to Bob, because I know Bob will talk about all the unique features we are putting into the product candidate. Let's keep it to what we've publicly disclosed.

Sure, thanks, Scott. And obviously, we're very excited about the ability to put multiple things and we are going to add a couple of more components. And we'll be talking about those things later this year at this conferences in the second half of the year, but expect some added bells and whistles to CAR B7H3 program beyond what we have today to add further attributes for the purpose of going to solid tumor settings.

Okay. Thank you very much.

I would say generally, therefore, where we're starting in solid tumors, is building off of the FT538 backbone, which already has three edits and includes the CD16 receptor.

Your next question comes from the line of Mara Goldstein from Mizuho.

A question on the BCMA program in multiple myeloma and I'm just wondering how you view what will ultimately be the true competitive landscape for the programs on the NK side that you're working on relative to what we see currently in the clinical marketplace today.

I think that's going to continue to be a significant amount of innovation in the myeloma space. And obviously, we are partnered with Janssen, who is a company that has arguably the leading franchise in myeloma and has probably at least today a best-in-class CAR BCMA product candidate, if that is patient derived. So I do think the landscape in myeloma, given the very nature of that disease is going to lend itself to off the shelf treatment. I think it's going to lend itself to duration of therapies. And I do think it will lend itself today, given there are relapse rates that are still meaningful and significant to a multi-pronged approach to the disease, including embedding multiple mechanisms of action within the cell therapy. I mean, if you look at today, myeloma, it's littered with combination therapies, which bring multiple mechanisms actions to attack the plasma cells. I think long-term as you think about how you attack myeloma and potentially try and cure it, it's going to take multiple mechanisms of action. And so that's one of the things we're super excited about -- with a cell therapy approach, especially IPS derived. You can embed those multiple mechanisms of action within a single modality, the cell therapy.

Okay. I'd like to just ask what you're thinking for this year in terms of your approach to releases data, exiting last year, you had said that you would wait till you have, sort of critical mass and cohorts. So how are you guys thinking about it this year?

Sure, I'll let Ed tackle that.

Yes. We're trying to consolidate things into a more manageable digestible format of disease areas. And so similar to what we did at ASH this year around CD16 biology, I think you'll see us do a disease oriented approach. And I think there is four major milestones to look forward to in 2021. The first one is likely to be around AML where we get into late spring or early summer we have both FT516 and FT538 now dosing patients in AML. So we'll have some updates from those programs, call it by middle of the year. Shortly thereafter, we'll probably revisit lymphoma where we have both FT516 in combination with Rituximab, as well as the ongoing monotherapy in combination with Rituximab for FT596. The third major milestone will probably come in the third quarter and it'll be emphasizing solid tumors where we have FT500 ongoing in an expansion. And we're making good progress there, as well as what Scott mentioned in his prepared remarks around FT516 in combination with Avelumab. We also may have an opportunity to talk about the IND filings that we also referenced around FT536, our MICA and MICB program, as well as the progress we're making with Janssen and again in Amgen, it's not been disclosed, but we'll plan to file an IND. So we have quite a bit going on clinically, but also preclinically in terms of new innovation around solid tumors that we'll talk about in the third quarter. And then lastly, and fourthly around ASH, we'd like to have a good presence in multiple myeloma with FT538 in combination with daratumumab and then a small but hopefully good number of patients in FT576, for which we clear the IND at the end of last year and will begin to those patients as we get into the second half of this year. So quite a bit going on clinically focused on disease areas. And as we get into the fourth quarter with ASH specifically, we could use it as an opportunity to revisit lymphoma, or additional data as well. So lots of clinical data set for 2021 around [14] [ph] times of the year beginning, mid-year with AML.

As well as AML at ASH potentially too.

Next question is from Matt Biegler from Oppenheimer.

So, maybe I missed this but if you could just maybe walk me through 596s planned protocol amendment in terms of dosing? Is there going to be the same dose you have now divided out over several infusions? So I know you're on 90 million. Now, would it be like, let's say 30 million over three doses and I guess what you're doing with 516 and 538 or just any color you can give there might be helpful.

Yes. I think our plan would be to the dose level where currently cleared on, we would begin multi-dosing that clear dose. So if we're cleared, for instance, let's just pick 90 million cells. Let's say we're cleared 90 million cells as a single dose, we may have a protocol where it's three doses of 90 million cells each.

Oh, okay. Interesting. That's great. Cool….

I mean, if you go back, I mean, the analogy is, if you look at the 819 protocols that we have, where the 819 protocol has single dose and multi dosing, as well as the 576 protocol that has single dose and multi dosing, you essentially clear a single dose level of say, pick it 100 million cells. Once you clear that single dose level of 100 million cells, you can begin multi dosing with that cleared dose level. So you could do 2 100 million cell doses.

Got it. That make sense. Then I had maybe more of a subjective question. But have you noticed any up tick in patient recruitment or investigator interest in your trials following the ASH data set? Obviously, a lot of the indications are going after are pretty competitive in terms of investigational therapies. So just, any type of subjective insight you have would be helpful?

Yes. I definitely think we've seen a lot of interest and there has historically been a lot of interest in our IPS derived cell therapy programs. Part of the challenge that we deal with today is, we are in dose escalation. So we're gated right by how fast we can potentially move. So, today we're focused on a core number of sites that we think can help us manage through dose escalation in efficient way, but obviously, once we get to dose expansion play for instance, like with FT516, we have the potential to open up that -- to open that up much more broadly. And yes, we think there's significant interest there.

Next question is from Ben Burnett from Stifel.

This is Carolina Ibanez Ventoso on for Ben Burnett, thank you for taking our questions. I was wondering, can you provide any color on the type of high risk patients been enrolled into the University of Minnesota relapsed prevention study? And when might we get a look at clinical data there?

Sure. Wayne, do you want to take that? I mean, with respect to clinical data? I mean, I'll jump on that. Obviously, it's an investigator initiated study. So we'll work with the University of Minnesota with respect to clinical data. I would not expect clinical data before ASH, though on that program at the earliest given that the study is a relapse prevention study. But go ahead Wayne.

Yes. With respect to the study design, the way it goes is that patients with high risk B cell lymphoma and these are patients that have relapsed or there are refractory from their initial therapy. And then these are patients who otherwise would undergo high dose chemotherapy, followed by autologous stem cell transplant. And so the design of the study is essentially to take that high dose chemotherapy followed by autologous stem cell transplant and then add the combination of FT596 plus rituximab following transplant. And so that's where the relapse prevention comes from because we know historically that patients who undergo autologous stem cell transplant, at least half of them will still have relapsed disease following transplant. And so one of the primary endpoints for the study is essentially relapse free survival to see whether or not we can increase the percentage of patients who are relapse free, after following autologous transplant.

Okay, got it. And then, we haven't seen much evidence of CRS or neurotoxicity with regarding NK cells of lymphoma, do you take a similar result with current NK in the multiple myeloma setting?

This is pure speculation. Go ahead, Wayne.

It's pure speculation, of course, but I think that we have been encouraged by what we have seen with other NK cell product candidates, particularly those in lymphoma, where in contrast, to CAR T therapies that are targeting the same antigen and CD19. We certainly don't see the frequency nor the severity of cytokine release syndrome or neurotoxicity have been observed with CAR T. And as Scott mentioned, in our FT516, and FT596 dated today, we haven't seen any grade CRS or neurotoxicity. So, for what it's worth, we're encouraged by that and we hope to see the same pattern in our myeloma programs.

Next question is from Biren Amin from Jefferies.

Maybe on 538. With a combination with dara and multiple myeloma, I think you stated that first dose at 100 million cells in patients who have failed at least two lines of therapy. Can you just talk about, I guess, prior lines of therapy because typically, I guess, in, with the BCMA CARs, we're seeing a median of about five or six lines of therapy. Are you expecting patients at third line in that trial? Or would you expect more refractory patients, and this is just simply like the inclusion criteria?

Sure. Go ahead, Wayne.

Yes. So, I mean, it's a fair question. From an eligibility standpoint we say that patients, have to have received two prior lines of therapy not just with respect to standard myeloma agents, such as a proteasome inhibitor and so on and so forth. But I think realistically, as we begin to enroll patients on this trial, at least initially, we would expect to see patients who received more than just two prior lines of therapy and we'll probably be seeing a patient population akin to -- but what has been enrolled with respect to the BCMA directed CAR T therapies.

Okay, that's helpful. And then, you mentioned the focus on the T cells earlier, Scott. Can you maybe just give us a status update on FT819? I think the IND cleared last July, on clinicaltrials.gov, the design was up in November. I guess, what are the steps you need in order to achieve patient dosing? And then, a question off of that is, there was a paper I think last month from Takeda researchers, I think lead authors, Eric Gucci, talking about, just iPSC cell differentiation for T cells and talked about, I guess, challenges with CD4s in particular versus CD8. I'm not sure if you saw that paper but if you could maybe comment on your efforts. And what you've seen with differentiation on CD4s versus CD8s.

Sure. Bob is nodding his head. So I'll let Bob answer the second question. The first question is, we've completed the first manufacturing run for 819. We're currently doing product release testing on that batch that we manufactured. Obviously, getting to the point you're making and Bob will discuss, we think there's obviously continued opportunity for process improvements with respect to developing out really high quality alpha beta T cells. And we're working on some of those improvements in parallel in real-time, including under our collaborations with ONO and Janssen. And we have kicked off a second manufacturing run where we've implemented those improvements. And so we're continuing to do a little bit of work assessing the improvements and we've guided that we will enroll the first patient in the middle of this year.

A follow up Scott's point, obviously referring to the nature communication study, where they took T cells and the reprogram. So there was no TCR engineering. And they had the -- even though they had challenges, they actually took a shortcut, because they had the opportunity to just have the endogenous TCR that they can take advantage of. What we've done over the past four or five years with Michel Sadelain has been basically coming up with a strategy where you don't have the TCR available, because we're going into an allogeneic setting and how to mitigate TCR signaling with a CAR. And that's where we put the CAR on the track locus, it turns on, [indiscernible] out of places and in a temporal manner gives us the signal we need for T cell selection. So it's a very complicated process. To your question about a CD8s and CD4s, the composition of our FT819 is a CD8 product. It is a very highly effective cell population. The CD4 compartment it's always been discussed as a helper population. And that population you need for long-term persistence when you have a single dose. So here in a multi dose manner, we feel that the CD8s are the proper dosing strategy for our first product. We are actively working on making CD4s on the side, but CD8s are the focus of FT819. So basically, that's our strategy mix CD8, carrying the CAR and make CD4s in a different timeline.

Your next question comes from the line of Peter Lawson from Barclays.

The AML data we get kind of mid year-ish, is that going to be kind of ASCO or is it kind of like a press release? What's the plan around that?

We'll continue that what we've done in the past, I mean, whether it will be part of a conference agenda, or we will do it alongside the conference, like we did at FT516 at ASH. We'll do it as part of a scientific conference. We're not just going to do as part of just a one off press release. We'll announce it as part of some type of event.

What's the best buy there for 516 and 538 in AML? Is it you kind of want to be on par with the hallow kind of approaches for NK cells?

Historically, I think, he look, I think people have been honestly excited about some of the complete responses that have been generated in AML, and again, relapsed refractory AML. These are patients that really don't have any great options. And they're not in a position given the state of their disease where they can go on to transplant. And so, we're certainly looking at and we talked about the limitations with donor derived NK cell therapy that wasn't really scalable given some of the limitations. And so, if we can come in with an off the shelf cell therapy, achieved CR, CRI rates of 20% to 30% drive patients to leukemic free state where they can bridge the transplant with an off the shelf product candidate. I think that's a great option. And I think there's really a meaningful therapeutic impact that you can have for patients with relapsed refractory AML if we can achieve that. I do say I will stand by, the comment I made earlier, though, long-term, if you start thinking about long-term AML, yes, you will have engineered targeted strategies.

Okay. And then, just generally, as we kind of think about repeat dosing, do you think on repeat dosing, there's going to be an increased chance of graft rejection essentially?

It's an interesting question. I mean we look at this for every single patient that we treat across any of our programs, 500, 516,596, 538 I mean, we look for this. We have not seen Tier B cell mediated rejection arise. Now, it's a fair question, as you go out further on the curve and further out from conditioning, as you do more rounds of conditioning, will that arise? It's a fair question. And it's something as sort of Wayne alluded to, we're interested in investigating including comparing it to non Cy/Flu conditioning regimens.

And my next question, do you think we can get away from Flu/Cy conditioning?

I think we're going to begin investigating that in pretty short order.

Your next question comes from the line of Nick Abbott from Wells Fargo.

So Scott, you probably created over 40 patients now in FT500 series of trials, can you talk a little bit about the clinical protocol logistics, I mean there's an obvious need for bridging therapy, presumably, but that would rely on the fact that everything goes well, and the cells are there and the patients get the Flu/Cy on time. And then, of any patients required hospitalization before or immediately after for treatment related AIE. I know the cells are given in the outpatient setting. But I'm just wondering about rates of hospitalization. And I have a follow up.

Wayne can talk about this sort of what we've seen in preparing patients, I mean, we've seen very little utilization of or need to use a sort of a bridging strategy, given the cells are there, they can be administered off the shelf. We obviously never discussed hospitalization rates, but most of our product candidates are designed for the protocol to be delivered in the outpatient setting. I will say, though, there are certain centers, when they treat the first patient, for example, or the first second patient at that center, where they do initially require hospitalization for a short period of time, just because it's the first time with respect to the therapy.

Yes. I mean, I think just to add to that in our cumulative experience to-date, we have virtually no instances where a patient received, co-bridging therapy, where the reason for administering that bridging therapy was to buy time until FT series of cells were made available. So, it was really -- in most cases, as exemplified by what we discussed earlier, patients who are refractory from their last therapy, as soon as they become eligible for the study, they come on to the study, they get their Flu/Cy and they get themselves, they've not had to have, a single agent chemotherapy as a tie over. So that is almost -- that's virtually non-existent in our experience to-date. And then, as far as hospitalization is concerned, I think one thing that's worth reminding is that, to-date we have not seen any serious adverse events that are attributable to any of the cell products, which means that in virtually all cases, patients who require hospitalization during the treatment period, they're hospitalized for things other than effects of the cells and it's most often due to the patient's underlying disease, as well as in some cases, effects from the Flu/Cy conditioning, which are expected given what we know about the safety profile for that combination.

That's helpful. And for the expansion cohorts, it sounds like at least in some of them, you're going to do some additional exploration of dose and as you mentioned, lympho conditioning. Are you going to begin to focus on specific cohorts and I'm thinking of AML, where you could have a cohort of primary induction failures, early relapse, or even non elderly frontline patients who are ineligible for intensive induction therapy?

Yes, absolutely. I think that is absolutely an opportunity in AML. Certainly, given the different lines of therapy, I think, where we will absolutely start to -- you'll start to see this as with FT516 in lymphoma where today we have the most flexibility given we are at the highest dose level and give it the safety and efficacy profile we've seen to-date.

Okay, thanks. And then just last one, you mentioned that there are some improvements for 819. Are you going to complete this second batch before you decide which to use in the middle of the year?

Yes, we probably will. I mean, we've done a lot of work on the first batch. And we're actually very comfortable with the in vivo efficacy we're seeing from the first batch. But like I said, we're always innovating. We have implemented some process of improvements on the preclinical side and preclinically they do make a difference. So we are going to take a look at the second batch.

Okay. And then by extrapolation and should we assume the -- not felt the need to do that with the NK portfolio?

With the NK portfolio, we have definitely made process improvements over time. But this was a situation where we were making a process improvement in real-time before we had treated the first patient. There was an element of innovation that occurred prior to treating the first patient.

That is your last question presenters, you may continue.

Perfect. Thank you everyone for participating in today's call, best wishes.

Thank you all for your participation in today's call and your continued interest and support of Fate Therapeutics. Be well. You may know all disconnect.