Postprandial lipemia is traditionally defined by the extent and duration of the increase in plasma triglycerides in response to a fat-enriched meal. The relationship between alimentary lipemia and coronary disease is of great interest in view of the epidemiological and experimental evidence that underlies it. The rate of synthesis of triglyceride-rich lipoproteins, lipoprotein lipase-mediated triglyceride hydrolysis, and the hepatic capture of chylomicron remnants via the interaction of the lipoprotein receptor with APOE and LPL, are the fundamental pillars of the metabolism and modification of these lipoproteins. The modulation of such phenomena is influenced by both genetic and environmental factors, thus explaining their extraordinary individual variance. This review presents the current evidence linking a number of candidate genes to the modulation of postprandial lipid metabolism.