This hyperestrogenic state, combined with obesity-associated insulin resistance and hyperinsulinemia, activates key oncogenic signaling cascades such as phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) and Signal Transducer and Activator of Transcription 3 (STAT3), ultimately driving endometrial hyperplasia progression toward malignant transformation [4,5,6]. The gene discussed is AKT1; the disease is hyperinsulinism.