Notably, common oncogenic KRAS mutants such as G12V and G12D were not recalcitrant to phosphorylation-mediated regulation, and pharmacologic inhibition of SHP2 led to the accumulation of silenced pKRAS, supporting the potential clinical utility of manipulating the Src- and SHP2-mediated phosphorylation cycle of KRAS in the management of KRAS-driven cancers. This evidence concerns the gene KRAS and cancer.