One strategy for targeting KRAS‐driven tumors is to exploit collateral damage contextually induced by a mutant KRAS, in light of the concept that mutant KRAS alters physiological biochemical networks and induces cellular stresses (genotoxic, proteotoxic, and metabolic), rendering KRAS‐mutant cancer cells particularly reliant on stress‐remedy signaling for survival (Luo et al, 2009; Downward, 2015; Nagel et al, 2016). This evidence concerns the gene KRAS and cancer.