Previous studies have suggested that alterations in the PI3K/AKT/mTOR pathway are strongly implicated in endometrial cancer pathogenesis, and targeting the effectors of this pathway is a rational therapeutic approach.[27] We transduced genetic alterations of the key genes in the PI3K/AKT/mTOR pathway in these four EC tumors, including Pten deficiency, Pik3r1 deficiency, and Pik3ca E545K amplification. The gene discussed is MTOR; the disease is endometrial cancer.