Insulin, as a cell growth factor, activates phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) and mitogen-activated protein kinase (MAPK) signaling pathways, prompts angiogenesis and prompts tumor proliferation (39); non-hyperinsulinemia pathways include the estrogen or androgen imbalance caused by increased aromatase activity in adipose tissue of obese patients, the enhanced effects of adipokines and inflammatory factors, and increased thyroid-stimulating hormone (TSH) levels, etc. (40–43). The gene discussed is AKT1; the disease is hyperinsulinism.