In line with this, transcriptomic upregulation of basal markers is observed in prostate adenocarcinoma cell lines after the sole inactivation of TP53 and RB1. 51 Similar results were obtained in a preclinical model leveraging human prostate epithelial cells with concurrent inactivation of TP53/RB1, as well as overexpression of MYC, BCL2 and a constitutively active AKT isoform.68 Engraftment in vivo of such cells leads to the formation of tumors again exhibiting multiple histologies such as adenocarcinoma, squamous, small cell carcinomas, and mixed phenotypes. The gene discussed is TP53; the disease is prostate adenocarcinoma.