Of these, selection for the deletion of PTEN (phosphatase and tensin homolog) occurs in approximately 30% of prostate cancers, as lowered levels of PTEN increase the availability of phosphatidyl-inositol 3, 4, 5 triphosphate (PIP3) for driving PI 3-kinase (PI3K)-dependent signaling, such as cellular growth pathways downstream of AKT (protein kinase B) [7, 11]. This evidence concerns the gene AKT1 and Familial prostate cancer.