TP53 and neoplasm: Indeed, because the “metabolic transformation” of cancer cells commonly involves the oncogenetically driven addiction to nutrients (e.g., glucose) in the presence of genetically or functionally inactivated metabolic checkpoints, such as p53 deficiency, AMPK inactivation, and/or mTOR hyperactivation [71-73], it is not entirely unexpected that metformin-induced AMPK “re-activation” may induce specific tumor growth-inhibitory effects.