The interaction between the liver and other organs, such as the adipose tissue and intestines, leads to the progression of NAFLD/NASH; specifically, increased oxidative stress due to increased lipid influx to hepatocytes, promotion of insulin resistance, abnormal secretion of adipocytokines from adipose tissue, and endotoxin influx from the intestinal tract may be associated with the simultaneous development and progression of NAFLD/NASH [28]. This evidence concerns the gene INS and metabolic dysfunction-associated steatotic liver disease.