Postprandial lipemia (PPL) is characterized by the accumulation of triglyceride-rich lipoproteins (TRLs) and their partially hydrolyzed products that results from the absorption of digested dietary lipids in the form of chylomicrons (CM) that contain ApoB48 and/or increased hepatic production of very low density lipoproteins (VLDL) that contain ApoB100 [1]. Here, APOB is linked to hyperlipidemia.