KRAS glycine 12 mutant (KRASG12X) NSCLC and PDAC are thought to be particularly addicted to oncogenic RAS signaling, exemplified by KrasG12D inactivation studies in genetically engineered mouse models (6), pharmacologic inhibition of KRASG12D in preclinical models (7, 8), and most recently illustrated by the clinical activity of KRASG12C inhibitors in patients, leading to regulatory approvals for monotherapy in the treatment of patients with advanced KRASG12C mutant NSCLC (9, 10). The gene discussed is KRAS; the disease is non-small cell lung carcinoma.