Insulin resistance is implicated as a major player in the pathogenesis of NAFLD, and impaired suppression of adipose tissue lipolysis by insulin may lead directly to systemic free fatty acid overspill from adipocytes, with accumulation of intrahepatic diacylglycerol and triacylglycerol, as well as likely direct hepatocyte injury [51]. This evidence concerns the gene INS and metabolic dysfunction-associated steatotic liver disease.