LECT2 (leukocyte cell-derived chemotaxin 2) is a 16-kDa secreted hepatokine with pleiotropic functions in inflammation, fibrogenesis, and metabolic regulation 1. Primarily produced by hepatocytes, LECT2 exhibits neutrophil chemotactic activity and promotes chondrocyte proliferation 2. LECT2 functions through multiple cell surface receptors including Tie1, CD209a, and Met to regulate diverse pathological processes 3. Mechanistically, LECT2 binding to Tie1 interrupts Tie1/Tie2 heterodimerization and activates PPAR signaling, inhibiting endothelial cell migration and tube formation 4. In alcohol-associated hepatitis, LECT2 binds prohibitin 2 (PHB2) on neutrophils, disrupting PHB1/PHB2 complexes and promoting reactive oxygen species accumulation and neutrophil activation 5. Clinically, LECT2 is implicated in liver fibrosis, kidney fibrosis, ischemia-reperfusion injury, atherosclerosis, rheumatoid arthritis, hepatocellular carcinoma, and systemic amyloidosis 3. Elevated serum LECT2 correlates with advanced liver fibrosis staging and alcohol-associated hepatitis severity 4, 5. LECT2-knockout mice show attenuated fibrosis and reduced liver injury across multiple models 4, 6. AAV-mediated Lect2 shRNA knockdown demonstrates therapeutic potential for fibrotic diseases and hepatic ischemia-reperfusion injury 4, 7. Serum LECT2 levels represent a promising biomarker for disease screening and diagnosis, while LECT2 inhibition emerges as a therapeutic strategy for fibrotic and inflammatory conditions.