Troy Wilson: Yeah, Li, so the sort of a follow-on from €“ thank you for the 2 questions. A bit of a follow-on from Peter’s question. So what we’re waiting for is just is the site activation and steady startup over the last several years, it’s just taken longer to get sites up and running, I think not only in oncology, but in a number of disease areas. That’s just €“ they’re overloaded. They don’t have enough staffing. I mean, we all sort of know what’s going on. Our sites are very motivated, they are very engaged. We’ve had no challenges at all in getting sites interested to participate, now in 3 potential studies, the registrational study 001, the 007 and the 008. And I should have commented in response to Peter’s question, we actually will have European sites on the 001 study.
They’re just going to come online a little bit later than the U.S. sites. Li, as you know, we’re basically what we’ve tried to do with the strategy with 007 and 008 is to make the funnel as large as possible, so that any potential patient with KMT2A or NPM1 on any regimen is eligible to come into 1 of those 2 trials. That’s one of the ways we’re looking to really maximize the value of ziftomenib in AML, and that’s really resonated with investigators. It’s likely, of course, that the venetoclax containing regimens will probably go more quickly, because that’s €“ those are the largest number of patients. But, we’re going to open the cohorts as quickly as we can. With regard to your question around timing, I’ll just repeat what I said to Peter, that the focus is very much going to be on a mid-year clinical update in the NPM1 population.
And then as soon as it’s appropriate to provide an update on the combo either the KMT2A or the NPM1, we’ll look to do that in some form and fashion. I just can’t be any more specific because, again, the team is just cranking on getting the trial sites open, and the first patients on the study.
Li Watsek: Thank you.
Troy Wilson: Sorry, and one other additional point that I’m just reminded of. Just for everybody’s benefit, we can of course combine data on KMT2A regardless of the combination regimen to show the mitigation of differentiation syndrome. So it’s not as though we have to wait for any one of those cohorts to enroll. They certainly the expectation is the combination will mitigate the signs and symptoms of differentiation syndrome. And we’ll look to show that it’s just with us not yet having patients on study, it’s a little hard to do. The crystal ball isn’t as clear as I’d like it to be.
Operator: Our next question is from Brad Canino with Stifel. Please proceed with your question.
Bradley Canino: Great. Thanks for the question. And Troy, it’ll really be a follow-up to what you just said. Because, I just want to get your working thoughts on the zifto combination data and how quickly you think they can be used to serve as evidence that DS can be mitigated. And really, it’s a question of sample size. Do you think it would only take a handful of KMT2A patients to show that DS is lower and that you can drive those patients towards a response? I think the corollary there is on efficacy, how do you then think about parsing the contribution of efficacy from the components with a small end in that scenario?
