Since LPL plays an important role in VLDL metabolism by hydrolyzing its core TG, its inhibition can lead to hypertriglyceridemia and diminished postprandial clearance of TG-rich lipoproteins mainly due to increased apolipoprotein C-III (apoC-III), which interferes with the binding of apolipoprotein B (apoB) and apolipoprotein E (apoE) to hepatic receptors [14,46,47]. The gene discussed is APOC3; the disease is hypertriglyceridemia.