Considering identification of pathophysiological mechanisms underlying NAFLD incidence and remission, we also acknowledge related limitations in our study as our analyses did not include genetics, measurement of adipose tissue insulin resistance index by means of a product of fasting plasma insulin, and free fatty acid concentrations or estimation of hepatic de novo lipogenesis with specialized methods like fatty acid profiling and isotope tracers (18, 80). This evidence concerns the gene INS and metabolic dysfunction-associated steatotic liver disease.