The insulin resistance initiates the induction of hyperinsulinemia and enhances the expression of proinflammatory genes encoding for factors such as cytokines and chemokines via Akt/FoxOs axis downregulation and NF-κB activation, leading to age-related inflammation (senoinflammation) in non-metabolic organs (Fig. 1). The gene discussed is AKT1; the disease is Insulin resistance.