Indeed, the phosphorylation of S6, 4E-bp1, and Akt, the downstream effectors of the mTORC1/2 pathways, were all significantly increased in the prostate tumors from Deptor−/−;Pten+/− mice, as compared with those from Deptor+/+;Pten+/− mice (Fig. 6d). The gene discussed is AKT1; the disease is prostate neoplasm.