The phosphatase and tensin homolog deleted on chromosome 10 (PTEN), a negative regulator of PI3K/Akt/mTOR signaling, has been originally discovered as a tumor suppressor mutated and lost in various cancers [7] and the consequential increased PI3K activity is associated with a high Gleason score and with advanced pathological stage disease, suggesting a pivotal role of PI3K pathway in HRPC [8, 9]. This evidence concerns the gene AKT1 and neoplasm.