Given the high levels of RS and DNA damage in treatment-naïve and on-treatment KRAS-mutant cancer cells, we hypothesize that the combination of KRASG12C inhibition with azenosertib, a novel, selective, and orally bioavailable inhibitor of WEE1 (37), could capitalize on these inherent vulnerabilities and result in combination benefit in KRASG12C cancer models. This evidence concerns the gene KRAS and cancer.