Indeed, VLDL-R-deficient mice have reduced LPL activity because the VLDL receptor is involved in the translocation of LPL from cardiomyocytes to the endothelial surface [55], causing hypertriglyceridaemia associated with reduced catabolism of VLDL-TAG by LPL. The gene discussed is VLDLR; the disease is hypertriglyceridemia.