LIPF encodes a gastric lipase that catalyzes the hydrolysis of triacylglycerols into free fatty acids, diacylglycerols, monoacylglycerols, and glycerol, with preferential activity at the sn-3 position of the triglyceride molecule. The enzyme is localized primarily to the fundic region of the stomach and requires its N-terminal tetrapeptide for lipid binding and function. During fat digestion, gastric lipase contributes approximately 10–17.5% of total triglyceride hydrolysis in vivo, remaining active in the duodenum where it participates in nutrient absorption 1. LIPF expression is significantly reduced in gastric adenocarcinoma tissues compared to normal tissue, with downregulation observed in 59.1% of cancer samples versus 94.4% of normal samples 2. Recent genomic studies identify LIPF as a chief-cell marker expressed in a distinct subtype of fundic gland-type gastric adenocarcinoma and as a serum biomarker for early gastric cancer diagnosis when combined with other proteins 3, 4. Additionally, LIPF expression correlates with better overall survival outcomes in gastric cancer with bone metastasis 5. Genetic variants affecting LIPF have been associated with gestational diabetes mellitus risk in Chinese populations, suggesting a broader role in lipolysis-dependent metabolic regulation 6.