GPAT3 (glycerol-3-phosphate acyltransferase 3) is an endoplasmic reticulum-localized enzyme catalyzing the first and rate-limiting steps of glycerolipid biosynthesis 1. It converts glycerol-3-phosphate to lysophosphatidic acid (LPA) and subsequently to phosphatidic acid (PA), both critical intermediates in triglyceride and phospholipid synthesis 23. GPAT3 is predominantly expressed in adipose tissue and is dramatically upregulated (~60-fold) during adipocyte differentiation, where it represents the major GPAT isoform driving lipid accumulation 4. Its expression is regulated by insulin signaling and endoplasmic reticulum stress through ATF4-mediated AP-1 elements 5. GPAT3 activity is stabilized and enhanced by the cofactor CHP1, which facilitates recruitment of GPAT3 to lipid droplets 6. Clinically, GPAT3 upregulation contributes to sorafenib resistance in hepatocellular carcinoma by promoting triglyceride synthesis and activating anti-apoptotic NF-κB/Bcl2 signaling 7. In Kupffer cells, GPAT3-mediated LPA synthesis exacerbates inflammation through ERK pathway activation 8. Conversely, GPAT3 deletion ameliorates metabolic dysfunction in lipodystrophy models, suggesting GPAT inhibitors may have therapeutic potential for metabolic and malignant diseases 9.