LPCAT3 (lysophosphatidylcholine acyltransferase 3) is a phospholipid remodeling enzyme that catalyzes the reacylation step of the Lands cycle, converting lysophospholipids into mature phospholipids 1. Specifically, LPCAT3 transfers polyunsaturated fatty acyl chains from acyl-CoA donors to lysophosphatidylcholine, lysophosphatidylserine, and lysophosphatidylethanolamine, generating phosphatidylcholine, phosphatidylserine, and phosphatidylethanolamine respectively 1. In liver, LPCAT3 maintains systemic lipid homeostasis by regulating membrane phospholipid composition, particularly incorporating arachidonate into phospholipids that facilitate VLDL secretion and modulate ER stress responses 1. In intestine, LPCAT3 enables efficient lipid absorption and chylomicron assembly by regulating polyunsaturated phosphatidylcholine levels 1. Clinically, LPCAT3 dysfunction is implicated in nonalcoholic fatty liver disease (NAFLD) progression; decreased LPCAT3 expression correlates with NASH severity and impaired mitochondrial homeostasis 2. LPCAT3 also participates in ferroptosis regulation, with its upregulation promoting lipid peroxidation and enhancing anti-PD-1 immunotherapy efficacy in melanoma and lung cancer 3. Conversely, cancer cells evade immune-mediated ferroptosis by suppressing LPCAT3 expression through FABP7-driven epigenetic reprogramming 4. These findings suggest LPCAT3 modulation represents a therapeutic target for metabolic and immune-oncology diseases.