Let me try one more time, Maria. When you think about radiopharmaceuticals traditionally conceived, you’re infusing a radioactive compound systemically IV. And those radioactive compounds have certain affinities. So radium has affinity in places where there is calcium. So radium builds up in the bone. So you have systemic side effects. And if you don’t have a very targeted approach to all of where you find the relevant cancer because this is really infusing a radioactive agent. Radioligand therapy, which is what we do with Advanced Accelerator Applications and what we do here with Endocyte, links a scientifically well-understood ligand that’s specific to a specific cancer that links to a radioactive particle through conjugation chemistry. In the case of prostate cancer, there is a well-understood androgen called prostate-specific membrane antigen, PSMA, which is used as a diagnostic and ultimately used for treating the cancer. So what our aspiration is, based on all the science we understand, is that the these PSMAs are overexpressed on prostate cancer cell. So wherever you find prostate cancer in the body, you will be able to treat with radioligand therapy as that by Endocyte. Our expectation is we will be able to work well in bone met, but more importantly, we will work well for anywhere in the body that you find prostate cancer. And then we hope to create overall survival benefit and progression-free survival benefits in the indication of prostate cancer. And then on AVSX-101 as a foundational therapy, really, what I – what we believe, and we have to ultimately generate data to show there’s an SMA 2, 3. But on SMA 1, we’ve clearly shown this is the foundational therapy, potentially lifelong, clear and compelling efficacy, remarkable efficacy. And so far, what we’ve seen over the patients beyond four-year consistent effect. Now in SMA 2, 3, we have the studies running mechanistically, we believe correcting the SMN1 gene fundamentally is want you want to do here. And that’s what we’re trying to do with this and that should enable the speed of action and the hopeful clinical benefit that you want to see in SME type 2, 3. Now we need to show that. We believe gene therapy would be foundational in those patients as well. I mean, we always have to remind ourselves here that this is an absolutely terrible disease. You need patients who have these disease, if you meet their patients, this is an absolutely devastating condition. So having benefits that are quick, saving what motor neuron are available still in the body, enabling function has a huge, huge impact. So when we look at this from a distance, we start to say, well, these things look all very similar. Actually, these differences matter massively to the patients involved. So I think that’s what we believe will ultimately here today with respect to onetime gene therapy for these patients. So last question.