In the pathogenesis of NAFLD and NASH, an increase in plasma insulin levels, de novo lipogenesis, TG, and hepatic gluconeogenesis finally resulted in lipotoxicity, damage to hepatocytes, and an influx of immune cells, activation of transforming growth factor β (TGF-β)/SMAD signaling in hepatic stellate cells (HSCs), their differentiation into myofibroblasts, and finally proceeding to progressive fibrosis in the chronic state of NASH [61,62]. This evidence concerns the gene INS and metabolic dysfunction-associated steatohepatitis.