TG-rich lipoproteins, including very-low-density lipoprotein (VLDL), chylomicrons, and chylomicron remnants, start to increase in the early stages of CKD because of suppressed lipoprotein lipase (LPL)-mediated hydrolysis of VLDL and chylomicrons and an excess of lipase inhibitors such as apoC-III and pre-beta-HDL in uremic plasma (25, 26); these TG-rich lipoprotein remnants contribute to the initiation and progression of atherosclerosis (27). The gene discussed is LPL; the disease is atherosclerosis.