A significant proportion, approximately 93%, of Type I EC, specifically the endometrioid type, exhibit an absence of the phosphatase and tensin homolog (PTEN) or harbor mutations within the PI3K/Akt/mTOR pathways, which are associated with glucose metabolism, hyperglycemia stimulates changes in the above signaling pathways to increase the proliferation, invasion, and migration of tumor cells, so hyperglycemia is associated with deep myometrial invasion in patients with type I EC (26–28). The gene discussed is MTOR; the disease is neoplasm.