Their studies showed that the induction of KRASG12V, NRASQ61K or MRASQ71R (a small GTPase involved in regulating the dimerization and activation of CRAF, a signaling molecule of the MAPK-ERK pathway downstream of KRAS [95]) mutations in tumor cell lines containing KRASG12C mutations reduced the inhibitory effect of KRASG12C inhibitor sotorasib on downstream signaling and failed to significantly alter the level of endogenous KRAS activation. The gene discussed is KRAS; the disease is neoplasm.