I mean, for instance, if you look at perhaps in colon cancer, about 1/3 of them co-express a mutation in RAS problem.
Operator: Our next question comes from Jonathan Chang with SVB Securities.
Faisal Khurshid: This is Faisal Khurshid on for Jonathan. I wanted to ask if you could comment at all on pace of enrollment for the multi-RAS versus the muni-specific programs like the G12C. Do you expect one to go faster than another? And then do you also plan to provide any color as the study goes along on what your dose levels have been cleared?
Mark Goldsmith: Thanks for your question. In terms of pace of enrollment, they’re both doing fine. I think they’re both on track with expectations. What were our expectations? We’ll we expected that Pharmacy 6236 would have an abundance of patients and investigators highly interested because of the absence of approved targeted therapies in most of those indications and that’s what we’re seeing. We have very, very high demand for the fixed number of stuff that are available. But nonetheless, we are seeing enrollment in both of these studies I’m sorry and things are progressing per plan. Your second question was?
Faisal Khurshid: As the studies progress, do you plan to provide any color on what your dose levels have been cleared?
Mark Goldsmith: Not as an isolated bit of information. It probably won’t really mean much to anybody because these are entirely new compounds. Obviously, when we report some additional information about tolerability, safety and/or activity will provide dose information associated with it.
Faisal Khurshid: Got it. Okay. And if I could ask one more. Have you looked at how the chaperone protein levels change over time as you dose? Is this a dynamic thing? Or are these consistently expressed in the tumors?
Mark Goldsmith: Steve, do you want to comment on that?
Steve Kelsey: Yes. The chaperone proceed of interest is of cycle for day is hugely abundant in most mammalian tissues and circa human tissues and also in cancer. And so far, we have struggled very hard to detecting the meaningful change in the expression of cycle for the day over time with any given exposure to our RAS(ON) inhibitors. So we don’t expect that to be — we don’t expect that to be something that is going to be possible to detect in the clinic, even if we had an assay that could deal with the massive overuse of that process.
Operator: And our next question comes from Eric Joseph with JPMorgan.
Eric Joseph: Actually, a couple from us. So looking to initial data with 6291 next year, Mark, what would qualify as superior activity in your view relative to the RAS(ON) inhibitors? Is that a statement in the PR, that a function of PD or activity in RAS inhibitors prior RAS inhibitor-treated patients or perhaps better response rates in certain histologies? And to the extent it’s the latter, are there certain tumor types that you’re aiming to bias enrollment towards?
Mark Goldsmith: Yes. Thanks, Eric. I appreciate the question. I think as we start to collect data, the things we’re going to see initially will be safety and tolerability. And then from there, we’ll start to see — we expect a tumor activity. And obviously, objective responses are the things we’ll see earliest and durability is something we have to wait to collect that information. That’s not something you see early. Any combination of those, I think, will be helpful to us, keeping in mind that this is a new platform and so we often hear from investors that they simply want to see evidence that you can dose the patient, achieve exposure levels that should be active and then see activity from it. So that’s probably where things will start.
