It is well established that insulin-resistance-induced adipose tissue lipolysis and consequently augmented free fatty acid supply to the liver, together with the blunted suppressive effect of insulin on VLDL production and the decreased VLDL catabolism due to low LPL, are major causes for the increased serum levels of TG-rich VLDL particles and hypertriglyceridemia in MS (reviewed in [25,26]). The gene discussed is LPL; the disease is Insulin resistance.