The notion is supported by two reports showing that transgenic mice expressing Skp2 in prostate also develop prostate intraepithelial neoplasia (PIN) similar to Akt1 transgenic mice, and that Skp2 deficiency profoundly restricts prostate cancer and adrenal tumor formation upon PTEN inactivation [69, 70], suggesting that Skp2 is a critical player for PTEN/Akt-mediated tumorigenesis. This evidence concerns the gene PTEN and Familial prostate cancer.