VLDLR and steatosis: The disruption of the lipid homeostasis in the ER can trigger ER stress and subsequently activation of the unfolded protein response (UPR) (6–8), leading to de novo lipogenesis (9), reduced fatty acid oxidation, disturbed lipoprotein and very low-density lipoprotein (VLDL) secretion (10), and increases in VLDL receptor (VLDLR) expression (11) resulting in steatosis.