To parallel these findings in both indolent and aggressive forms of mouse prostate tumors, we took advantage of three classical genetically engineered mouse models of PCa, whereby the tumorigenic process in the prostate epithelium is driven by conditional loss of Pten (Pb-Cre4;Ptenflox/flox), Pten and Trp53 (Pb-Cre4;Ptenflox/flox;Trp53flox/flox), or the overexpression of the large T antigen of SV40 (TRAMP) [19,25,26]. The gene discussed is TP53; the disease is posterior cortical atrophy.