ApoA-V is involved in the regulation of plasma triglyceride levels. Thus, human apoA-V transgenic mice have lower triglyceride levels than controls, whereas the knockouts have increased levels. 1 Because hypertriglyceridemia is an independent risk factor for the development of atherosclerosis and cardiovascular diseases, elucidation of the mechanism behind the regulation of apoA-V is of great importance. Expression of apoA-V is increased by interaction of the heterodimer PPARα (peroxisome proliferator-activator receptor)/RXR (retinoid X receptor) with a “Direct Repeat” 1 (DR1) sequence in the apoA-V promoter. 3, 4 In this issue of