A common genetic event that contributes to cancer cell growth and survival is the activation of the PI3K/Akt pathway via PTEN loss-of-function.61, 62 In the late stages of the disease, PTEN loss-of-function and/or PI3K/Akt pathway activation is observed in 70% of prostate cancers.63 PTEN loss and subsequent PI3K/Akt signaling cause mTOR activation.64 mTOR regulates cellular metabolism by controlling glucose uptake, glycolysis, fatty acid metabolism and the pentose phosphate pathway.41 mTOR kinase exists in two signaling complexes, mTORC1 and mTORC2. This evidence concerns the gene PTEN and prostate carcinoma.