Atherogenic dyslipidemia associated with NAFLD is the consequence of increased de novo hepatic lipogenesis along with an elevated rate of lipid uptake, both mechanisms determining the overproduction and secretion of large triglyceride-enriched VLDL particles, including apolipoprotein C3 (ApoC3) and apolipoprotein B (ApoB). This evidence concerns the gene APOB and metabolic syndrome.