KRAS and cancer: Consistent with a functional role of KRAS Y96D, ectopic introduction of the mutant gene into KRAS G12C-addicted cancer cell lines attenuated the growth-suppressing effect of inactive-state KRAS G12C inhibitors and enhanced KRAS signaling, indicating that KRAS Y96D is an oncogenic mutation that leads to constitutive KRAS activation and imparts resistance to KRAS G12C blockage [48,49].