AKT1 and neoplasm: As a critical negative regulator, inactivating mutations or epigenetic silencing of phosphatase and tensin homolog (PTEN) impair its phosphatase function, causing abnormal accumulation of phosphatidylinositol-3,4,5-trisphosphate (PIP3) and sustained activation of the Akt/mTOR signaling cascade, ultimately fostering tumor proliferation and metabolic adaptation.