We have previously shown that Pten(i)pe−/− mice, in which Pten is inactivated in prostatic luminal cells at adulthood, develop prostatic intraepithelial neoplasia (PIN) due to enhanced proliferation of prostatic epithelial cells (PECs), featuring stabilization of p53, followed by a progressive growth arrest with characteristics of cell senescence. The gene discussed is TP53; the disease is prostate intraepithelial neoplasia.