In addition, it was recently reported that ER stress-dependent hepatic steatosis was diminished in the livers of the VLDLR-deficient and ApoE-deficient mice compared to the wild-type mice, suggesting that steatosis can be reduced when the availability of lipoproteins to deliver fat to liver, allowing intracellular triglyceride accumulation, is diminished [55]. This evidence concerns the gene VLDLR and fatty liver disease.