Michael Schmidt: Yes. All right. That makes sense. All right. Well, thank you for taking my questions and congrats on the data update today.
Mark Goldsmith: Thank you.
Operator: Our next question comes from Marc Frahm with Cowen. Your line is now open.
Marc Frahm: Hi. Thanks for taking the questions and congrats on the data and seeing that 6236 is active in the clinic. Maybe just a follow-up on one of the earlier questions to start. Steve, I think there’s 20 patients dosed at 40 milligrams and above in the AE table and then there’s 12 in the waterfall plot. Can you just explain those incremental patients? It sounds like maybe a few of them are colorectal cancer patients that you just don’t have enough to talk about monotherapy with. And then are there more patients who are just on study, but haven’t been scanned yet versus people who may have dropped out before the first scan?
Steve Kelsey: Yes. There’s far more patients on study that have not yet been evaluated for efficacy than there are patients with a colorectal counseling study. I was a little €“ I was deliberately vague about the other histotypes, but that’s because we will provide an update later in the year, which addresses that. But the reality is that the discrepancy is due to the speed at which the study is enrolling and the fact that patients have to be on study for six weeks before they get their first scan. So if you would model a whole bunch of patients within the last six weeks, they are evaluable for safety, but not for efficacy.
Mark Goldsmith: Yes. Well, and that’s the key, Marc, is that they’re on the table for adverse events or they’re considered as part of that calculation once they start dosing. But they need to be on study for six weeks before you get a scan.
Marc Frahm: Okay. That’s helpful. And then maybe just to the point of the preclinical modeling being pretty predictive. I guess, one, given the exposures you’re seeing so far, I guess, what dose level do you think might be equivalent to that 25 milligrams you tested mostly? And then also kind of related to that, is there any sign pre-clinically that G12D alterations might be maybe modestly more sensitive than the other alterations and makes sense that they would start responding first? Or do you think this is just kind of the noise in the system of seeing a lot of different tumor types and a lot of different mutations?
Mark Goldsmith: Yes. On the second question, not so much. I mean, when we €“ I think we shared data on the G12X versus non-G12X in various presentations, not necessarily corporate, but at some of the scientific meetings we’ve given a further breakdown. And without any doubt, the G12X as a group showed enrichment for higher sensitivity on average. But then you start to get in fairly small numbers, trying to compare D to B to A to F. In some cases, we only have a couple of models of one particular genotype right now there. So I don’t think we can say that today, and I don’t think we would conclude that D is more sensitive in the waterfall. It’s just not enough. Nine out of the €“ sorry, eight out of 12 are D in the waterfall plot and three are B and one is A. So it’s just really no way to determine sensitivity for that yet. We need to collect more information. Your first question was
Steve Kelsey: What place will we get to? What dose will we get to…?
Mark Goldsmith: Yes. Or how…
Marc Frahm: What if €“ given the exposures you’ve gained €“ you’ve got a fair amount of clinical exposure data now to start building the kind of the human model, not just the extrapolation from animals. But based on that, kind of where does that 25-milligram animal dose fall on? Is that 240? Is it 400 milligrams?
