In general, they reflect the universal processes of diabetic damage under the conditions of hyperinsulinemia and hyperglycemia: changes in the signaling of the Akt–AMPK–mTOR axis, induction of ER stress and epithelial-to-mesenchymal transition (EMT), inhibition of autophagy processes, generation and accumulation of ROS and AGE; under the influence of chronic hypoxia, an increase in hypoxia-inducible factor (HIF) activity, lipotoxicity, including inhibition of CREBP1 and FAS occurs. The gene discussed is AKT1; the disease is hyperinsulinism.