Similar to enhanced ethanol metabolism in the liver, Fru yields intermediates which are involved in the stimulation of prooxidative (ROS generation) and proinflammatory routes (via c-jun NH2-terminal kinase-1—JNK-1) as well as lipogenic factors (SREBP-1c), which in both cases result in hepatic IR and hepatic steatosis with possible further consequences (hepatitis, cirrhosis, and CCA) [39,40]. The gene discussed is SREBF1; the disease is fatty liver disease.