Short-term treatment with rapamycin in Pten+/− mice on a C57BL/6 background can suppress mTORC1 activity and inhibit the formation of prostate tumorigenesis, suggesting that tumor growth is mTOR dependent in this setting [223], and this anti-tumor effect is further supported by several independent studies in other Pten-deficient cancer models treated with rapamycin analogues [224,225,226,227,228]. The gene discussed is MTOR; the disease is neoplasm.