The most frequent altered pathway in endometrial cancer is the phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin (PI3K/AKT/mTOR) pathway.39 This pathway regulates key aspects of cancer biology, including cell growth and survival.67 Dysregulation can occur by many different mechanisms, including the inactivation of PTEN, which is the primary negative regulator, or mutations in PI3K3CA and KRAS. Loss of PTEN expression is frequent in (low-grade) endometrioid-type endometrial cancer with favorable prognosis. The gene discussed is AKT1; the disease is endometrial cancer.