mTOR can be activated by growth factors signal through the class I PI3K/Akt pathway, and inhibited by AMPK and p53.12, 13 Once activated, mTOR exerts a negative effect on autophagy by phosphorylating a complex of autophagy proteins (ULK1/2), which inhibits the downstream autophagy cascade.14, 15 In contrast, AMPK can suppress mTORC1 signaling to stimulate autophagy through TSC1/2 phosphorylation.16, 17 Several of the known tumor-suppressor genes (p53, PTEN, TSC1/TSC2) and tumor-associated genes (p21, AKT) also respectively stimulate or inhibit autophagy.10, 15. The gene discussed is PTEN; the disease is neoplasm.