The tumor suppressor PTEN negatively regulates AKT function; however, mutation in (or deletion of) PTEN either in primary (30%) or metastatic (63%) prostate tumors is often responsible for AKT-mediated survival signaling [14], resulting in downregulation of pro-apoptotic signaling governed by FOXO3a and Par-4 [15–17]. Here, FOXO3 is linked to neoplasm.