Unlike glucose, ingested fructose by-passes the rate-limiting step of glycolysis and is preferentially metabolized by the liver, where it stimulates hepatic DNL acting mainly through SREBP1c (sterol regulatory element-binding protein 1c) and ChREBP (carbohydrate responsive element-binding protein), inhibits the mitochondrial β-oxidation of long-chain FAs, induces endoplasmic reticulum stress, and promotes TG formation and hepatic steatosis (73, 110, 111). The gene discussed is MLXIPL; the disease is fatty liver disease.