And in terms of efficacy, certainly, it is designed as dose escalation in small cohorts of patients, but, of course, if there is a signal of efficacy, we’d be very pleased to have that information for updating in the second half later this year.
Daniel Wolle: Okay. Got it. One last question. With multiple KRAS inhibitors in development actually and on the market as you continue development of 3116, is there an opportunity for you to select the best fit partner as you advance into late-stage development?
Steve Hoerter: Yes. Thanks for the question, Daniel, with respect to KRASG12C inhibitors. And you’re right there are a variety of agents now, two approved in the U.S. And what we’re €“ as we’ve reported previously, the effect that we see with 3116 addressing autophagy is an escape when used in combination with the KRASG12C inhibitor is not specific to an individual KRASG12C inhibitor. It’s certainly a class effect. It’s a mechanistic effect that we see. So we’ve seen that and reported that preclinically, both with sotorasib, but also with at adagrasib. So there would be an opportunity going forward for us to consider additional KRASG12C combinations as we think about the ideal partner for a potential 3116 KRASG12C inhibitor combination.
Daniel Wolle: Great, thank you very much.
Operator: Please stand by for our next question. Our next question comes from Michael Schmidt with Guggenheim. Your line is now open.
Paul Jeng: Hi, good morning. Thanks for taking our question. This is Paul on for Michael. One from us on recruitment for the INSIGHT study. So your analysis sort of suggests that only a portion of GIST patients have detectable KIT mutations through ctDNA and there is some discussion at the ASCO Plenary about just as a relatively low ctDNA shedding cancer. So I just wanted to get your expectations on the speed of recruitment of patients for this target mutation population at INSIGHT once that study kicks off later this year and whether you anticipate any sort of challenges in that aspect? And then secondly, on 3116, maybe just provide some color on what drove your decision to combine with encorafenib and cetuximab and where you see that potential for the combination in colorectal cancer? Thank you.
Steve Hoerter: Yes, hi. Good morning, Paul. It’s Steve. So I’ll take the INSIGHT question that you posed and then ask Matt to speak to the 3116, encorafenib and cetuximab combination. So first, with respect to INSIGHT and enrollment in that study, we’ve now demonstrated very clearly the capability to enroll these large randomized studies in GIST globally. So we have a clear capability in terms of getting these studies up and running and enrolling them rapidly. With respect to patients with the specific mutation that we’ll be looking for patients who don’t shed ctDNA, this is a very similar fraction in GIST versus other solid tumors. So we don’t see that as being a differentiating factor. And with a simple blood-based diagnostic with a rapid turnaround time of 5 to 10 days, we don’t see that as being a barrier at all.
In fact, we see it as being an advantage to enrolling in the study. And then lastly, I would just offer that what we continue to hear from investigators and from thought leaders is a considerable amount of enthusiasm given the data that’s now been reported at ASCO for the potential of QINLOCK in the selected group of patients, and I think that’s going to serve as a real tailwind in terms of not only getting sites up and running, but also getting patients enrolled on study. Matt?
