It therefore seems an imbalance between the secretion of VLDL-triglyceride and VLDL-apolipoprotein B-100, resulting from a “failure” to sufficiently upregulate hepatic VLDL-apolipoprotein B-100 secretion to match the excess VLDL-triglyceride secretion, is central in the development and maintenance of NAFLD associated with obesity. This evidence concerns the gene APOB and obesity due to melanocortin 4 receptor deficiency.