It has been shown in the prostate-specific Pten-deleted mouse model of PCa that depletion of androgens significantly inhibited tumor growth progression without altering the activation of Akt and mTOR, however, the combination of antiandrogen treatment with rapamycin-mediated mTORC1 inhibition exhibited additive antitumor effects[94]. The gene discussed is AKT1; the disease is neoplasm.