VLDL overproduction and the decreased VLDL catabolism due to the low serum lipoprotein lipase (LPL) activity (secondary to low-grade persistent inflammation and insulin resistance) are the principal causes of the increased serum levels of TG-rich VLDL particles and hypertriglyceridemia in MS (reviewed in [6,7]). The gene discussed is LPL; the disease is Insulin resistance.