PTEN normally functions as a critical negative regulator of PI3K signaling; its inactivation in 80–95% of Type I endometrial carcinomas removes this crucial brake on pathway activity, leading to constitutive AKT activation that, when combined with hyperinsulinemia and IGF-1 pathway hyperactivity, drives aggressive cellular transformation characterized by uncontrolled proliferation, resistance to apoptosis, and enhanced survival signaling [1,4,36]. This evidence concerns the gene PTEN and endometrial carcinoma.