Transgenic mice expressing TRAP1 in the prostate developed epithelial hyperplasia and cellular atypia and, when examined in a Phosphatase And Tensin Homolog (Pten)+/− background, a common alteration in human prostate cancer, showed accelerated incidence of invasive prostatic adenocarcinoma, whereas deletion of TRAP1 delayed prostatic tumorigenesis. This evidence concerns the gene PTEN and prostate carcinoma.