RB1 and neoplasm: Mechanistically, these inhibitors induce tumor cell expression of endogenous retroviral elements through genome-wide retrotransposon hypomethylation—a process mediated by E2F-dependent suppression of DNA methyltransferase (DNMT) expression during Rb-mediated cell cycle arrest (Shen et al., 2025; Roulois et al., 2015).