Gilmore O’Neill: Yes. I think just building on Baisong’s remarks, as you’re obviously looking out towards the evolution of the market against the background of enthusiasm for our investigators and indeed the patients with the increase in our acceleration enrollment. We anticipate that in the future that the vast majority of patients will be awaiting dosing at the time of our launch, and I can go into more details on that. But I think, a very important point, I think something that has really resonated with the investigators is that our initial clinical data were very encouraging as presented in December, consistent with our preclinical data, and we’re actually very confident that we will see replication in subsequent patients as we continue to monitor them through the execution of the 301 studies.
Operator: Our next question comes from Steve Seedhouse with Raymond James.
Steve Seedhouse: My question actually requires a bit of a prelude, so I hope everyone can bear it for a moment. You made a comment on globin locus editing increasing fetal hemoglobin independent of erythropoietic stress. And as you know, ICER — the recent ICER report on exa-cel uncovered an ongoing phlebotomy, at least one in sickle cell and some of the earlier data releases for that program in thalassemia indicated phlebotomy use there as well, but that just stopped being reported at some moment. So it’s not clear how prevalent phlebotomy use is for exa-cel. And this is all important because there was data at ASH years ago, as I’m sure you also know, indicating BCL11A editing cooperates with phlebotomy and primates to accentuate F cells and ultimately HBF levels probably because of the stress erythropoiesis causes.
So all that said, I’m curious if you agree that phlebotomy is potentially confounding fetal hemoglobin data for BCL11A approaches. And if you know what is the impact specifically where your editing approach at the HBG1/2 locus, what has phlebotomy use been like in your study and if you think this is all potentially a competitive advantage for you? Thank you.
Baisong Mei : Steve, thank you very much for your question. So, from our own clinical data, preclinical data and also published clinical data, you’re probably referring to for the BCL11A targeting approach. It did require some stimulation for the erythropoietic stress to increase the fetal hemoglobin, sufficient fetal hemoglobin expression. And so, that’s actually the reason we’re treating the target we are treating now, and we actually did take longer time to get all the targets from a preclinical study perspective, and that’s been validated by other publications. And regarding specific clinical data for the BCL11A approach, I have not seen formal publication. So, I would be waiting for them to publish their data and so we’d have a better understanding. So I will not comment on their data unless published.
Gilmore O’Neill: However, it is worth pointing out that in our early disclosure, we actually noticed the combination of a very robust normalization or correction of anemia in our first patient in December. And that was associated with a robust fetal hemoglobin expression, suggesting that indeed stress erythropoiesis as we hypothesized based on the known biology and our nonclinical data, that our approach is not dependent on erythropoiesis.
Operator: Our next question is from Yanan Zhu with Wells Fargo.
