In cancer cells and biopsies, RB is usually inactivated by mutations or by nutritional stress through AMPK-dependent phosphorylation [158]; consequently, RB inactivation promotes cell cycle activation through E2F release (which in turn, induces the transcription of genes associated with the progression of G1 to an S phase in the cell cycle) and proapoptotic (BH3) protein depletion [159], favoring cancer onset and development. The gene discussed is RB1; the disease is cancer.