AKT1 and neoplasm: IR leads to glucose intolerance and compensatory hyperinsulinemia, which can promote tumor cell proliferation, inhibit apoptosis, and enhance metastatic potential through pathways such as the insulin-like growth factor-1 (IGF-1) and the phosphatidylinositol 3 -kinase/akstrain transforming/mechanistic target of rapamycin (PI3K/AKT/mTOR) signaling cascade (8–11).