In KRASG12C mutant cancers, the amount of GTP-bound KRAS proteins determines the sensitivity to KRASG12C inhibitors, which interacts with and blocks KRASG12C when it is in the inactive GDP-bound state (Figure 1), so an increased ratio of KRAS-GTP versus KRAS-GDP cause resistance to KRASG12C inhibitors (20, 57). The gene discussed is KRAS; the disease is cancer.