The contribution of PLA2G1B toward diet-induced hyperlipidemia and hyperglycemia appears to occur predominantly during the postprandial period due to the amount of lysophospholipids generated and absorbed during the digestion process.7, 8 Lysophospholipids influence lipid and glucose homeostasis by reducing mitochondrial fatty acid oxidation in the liver.8, 9 Another enzyme that modulates lysophospholipid availability and metabolism in the liver is lysophosphatidylcholine acyltransferase-3 (LPCAT3), a protein that catalyzes the reacylation of lysophospholipids to phospholipids. The gene discussed is LPCAT3; the disease is hyperlipidemia.