Mechanistically, a high level of ETV4AAA protein expression in prostate cells not only markedly alters the enhancer chromatin accessibility landscape, augmenting cell cycle progression, but also induces p53 and its downstream targets, including the cellular senescence programs, which underlines the molecular mechanism of mPIN regression in p53-wild-type and progression to prostate cancer with p53-loss in this murine prostate cancer model. Here, TP53 is linked to prostate carcinoma.