Based on our studies and published reports, we propose the following model of cooperativity between c-MYC and Pten in prostate cancer (Figure 7D): Overexpression of c-MYC initiates tumorigenesis by facilitating loss of Pten. The latter leads to the activation of the p53 pathway, which can result in either senescence or apoptosis depending on the predominant Trp53 target genes induced (i.e. cell cycle arrest genes e.g. p21cip1 versus pro-apoptotic genes e.g. PUMA, Bax etc.). This evidence concerns the gene CDKN1A and prostate carcinoma.