Indeed, exploiting cancer cell vulnerabilities contextually induced by mutant KRAS, in particularly the mechanisms critical for surveillance of oncogene-dependent cellular stresses (genotoxic, proteotoxic, and metabolic) that are permissive for strong oncogenic signaling, has not only provided promising therapeutic avenues but also a wealth of information on the fundamental principles of KRAS-induced tumorigenicity [12–14]. The gene discussed is KRAS; the disease is cancer.