Interestingly, we provide functional evidence for the role of E-cadherin in promoting the formation of primary and metastatic tumors in vivo, and we demonstrate that transient repression of E-cadherin in prostate cancer cells may be mediated by the PI3K/AKT signaling pathway as a possible consequence of increased Snail activity. The gene discussed is AKT1; the disease is Familial prostate cancer.