Similarly to the other forms of fatty liver, the transition of the disease in TASH could be determined by a progressive “two hit model”, with the “(multiple) secondary hits” occurring on the background of lipid deposition and consisting of the increase in oxidative stress, inflammatory cytokines, insulin resistance and mitochondrial dysfunction which produce inflammatory infiltration, fibrosis and hepatocytes necrosis typical of the steatohepatitis. This evidence concerns the gene INS and Hepatic steatosis.