Previous studies have shown that PTEN phosphatase negatively regulates PI3K/Akt signaling,34,35 but is frequently inactivated by a gene deletion or mutation, and also degraded in the proteosomes of many types of cancer cells.36 Various types of post-translational modifications, including phosphorylation, oxidation, and acetylation, are also known to regulate the function and stability of PTEN.37 In this study, we confirmed that endogenous NOS could mediate S-nitrosylation of PTEN and activate AKT/mTOR signaling, resulting in decreased levels of autophagy and increased chemoresistance. The gene discussed is AKT1; the disease is cancer.