Accordingly, ETV1 overexpression combined with loss of SMAD4 may be insufficient for carcinoma development, and future studies should focus on the analysis of, for instance, ETV1;Pb-Cre4;Smad4f/f;Pten+/− mice to examine whether SMAD4 loss allows overexpressed ETV1 to induce prostate adenocarcinomas in the context of more genetic changes. This evidence concerns the gene PTEN and carcinoma.