The excess of circulating FFAs and the consequent abnormal liver uptake and fat accumulation typical of NAFLD, derives from abnormal lipolysis (hydrolysis of triglyceride) in the adipose tissue, mediated by insulin resistance, which is the event responsible for the largest share of hepatic fat accumulation, increased de novo lipogenesis (starting from glucose or fructose), and excess in dietary fat intake (64, 66, 67). This evidence concerns the gene INS and metabolic dysfunction-associated steatotic liver disease.