Taken together with the report indicating the role of IRS-1 as the inducer of GCK and SREBP-1c, shown in rat hepatocytes [43] and liver-specific IRS-1 knockout mice [44], persistent expression of IRS-1 and hyperinsulinemia in NAFLD may enhance FAS upregulation in the steatotic liver. The gene discussed is FAS; the disease is hyperinsulinism.