Notably, changes occurring in the fatty liver of NAFLD could cause insulin resistance by altering paracrine and endocrine functions, which in turn would accelerate the development of NAFLD itself through impaired ability of insulin to suppress adipose tissue lipolysis, increased delivery of free fatty acids to the liver, and increased de novo lipogenesis [9], eventually triggering a vicious cycle between NAFLD and metabolic co-morbidities [10]. This evidence concerns the gene INS and Hepatic steatosis.