Gilmore O’Neill: Thanks very much, Linda. With regard to the percentage of fetal hemoglobin as a differentiator obviously we’re excited by the data we show its early days yet. And what is clear from the experience described for people who have coincident inheritance of hereditary persistence of fetal hemoglobin with sickle cell disease or indeed thalassemia is that the higher the level of fetal hemoglobin or percentage or fraction fetal hemoglobin the greater the benefit certainly for sickle cell disease. I’d say its 30 days for us, but Baisong, I don’t know if you want to answer that.
Baisong Mei: Yes, yes.
Gilmore O’Neill: I’ll come back to the third question.
Baisong Mei: Yes. Yes, thank you. Thank you, Yanan for this question. As Gilmore mentioned, we’re very pleased to see the fetal hemoglobin data as you refer to actually see patients over 50% and we are excited on that. It’s also because this is a rational design approach for EDIT-301. We compared that this approach of targeting the HBG12 promoter — with HBG12 promoter versus BCL11A we found that we have better fetal hemoglobin expression, but we are in the early stage. We actually want to see more data to physique and we’re looking forward to see more that ourselves on that.
Gilmore O’Neill: Thanks very much, Baisong. I think your final question was around the correlation between total hemoglobin and hemolytic markers. I think that is an interesting question before hand it to Baisong I’ll just remind one thing. While hemolysis is a critical part of sickle cell disease, the key driver we believe for driving total hemoglobin by design is enhanced erythroid production. Baisong if you want to add?
Baisong Mei: Yes, that’s exactly right, Gilmore. That’s what we’re going to say. I think what I want to mention that, we are very positive about our agnostic marker data on that. Then the — so the total hemoglobin level is related two aspects of that. One is hemolysis, one is HBG12 process. So I think in our design we designed to have this molecule have high fetal hemoglobin expression and it also so with the targeting of the HBG12 promoter, we have better actual [ph] process and better red blood protection. So we are looking forward to see more data on that. But we are very pleased with our hemolytic biomarkers.
Operator: Thank you. Our next question is from the line of Eric Schmidt with Cantor Fitzgerald. Please proceed with your question.
Eric Schmidt: Good morning. Thanks for taking my questions and congrats on the progress. Maybe the first, the HbF production levels are obviously quite impressive. Is there a total hemoglobin above which you start to grow concerned in sickle cell disease that patients have too much hemoglobin? If so, what that might be? And then maybe a follow-up for Caren. We saw a couple of large pharma gene editing deals this week. Perhaps you could comment on the overall level of interest in potential platform type collaborations. Thanks.
Gilmore O’Neill: Thanks very much, Eric. With regard to the total hemoglobin, we believe that correcting and that’s what we’ve seen hemoglobin physiology range is substantial benefit. I think we haven’t — we’re not going to — it’s hard to speculate about a level that is too high. Indeed, there has been an experience in general with polycythemia in sort of a broader patient population with some conflicting data about the risks of same. But as I say, we feel very confident about the data we’re getting with regard to a total hemoglobin and the way that we are correcting it to normal physiological ranges. I think you asked a question about some recent gene editing deals just this week that are announced. What I will say is that what is striking about is, it is great to see pharma, I say big pharma now in a period where we’ve seen some a dark of deals leaning in and increasing their excitement around the genome editing space.
In other words, what I would say is this has been a very good week for CRISPR genome editing space with both that sort of critical near to final step towards approval for a first CRISPR-based therapy and to see now pharma actually looking through the lens of substantial de-risking their view of the value of genome editing as they look to grow their portfolios. I don’t know.
Caren Deardorf: Yes. Thanks, Eric. It’s Caren. What I would add is I think Editas is so well-positioned right now, having refocused the portfolio, we are in a great place to be able to move our own programs forward and are very excited by the continued interest and it opens the door for partnering should that be the right path for us.
Operator: Our next question comes from the line of Steve Seedhouse with Raymond James. Please proceed with your question.
Steve Seedhouse: Good morning. Thank you. Two quick ones. First, are lymphocyte and neutrophil counts at baseline and post-transplant something that you are going to share in either the poster or the associated presentation at ASH? And then separately, is it your intent at Editas to commercialize EDIT-301 on your own? Thanks.
Gilmore O’Neill: Thanks very much for this question. With regard to neutrophil engraftment data, that is something that we actually did present at our EHA, and it would comprise or could be summarized in our presentations the end of the year, because it’s actually a measure of engraftment is part of the safety monitoring that we do in our studies. And then, with regard to your second question, which was around commercializing 301 on our own. Well, we actually look to commercializing 301. We’re actually building towards that because that we believe that’s important. We have indicated previously that we’re interested in an ex-U.S. partner with a large footprint. Obviously the details of any such partnership and how that might expand, would really depend very much on those negotiations. It’s something that we would share upon any kind of agreement, but only then.
