COLEC10 is a C-type lectin that binds preferentially to galactose, with secondary affinity for mannose and fucose. It functions as a pattern recognition receptor in the lectin pathway of complement activation and acts as a chemoattractant involved in cell migration regulation. COLEC10 is predominantly expressed by hepatic stellate cells in the liver, where it forms heteromeric complexes with the related collectin COLEC11. During craniofacial development, COLEC10 is expressed in the palatal basement membrane and, together with COLEC11 and MASP1/3, participates in neural crest cell migration essential for normal embryogenesis 1. Loss-of-function mutations in COLEC10 cause 3MC syndrome, an autosomal recessive disorder characterized by craniofacial abnormalities including cleft lip/palate, craniosynostosis, and hearing loss 12. In hepatocellular carcinoma (HCC), COLEC10 expression is reduced and inversely correlates with stemness markers; overexpression suppresses tumor-initiating capacity by inhibiting Wnt/β-catenin signaling and inducing endoplasmic reticulum stress via GRP78 binding 34. In chr8 liver disease, COLEC10 expression decreases with fibrosis progression, though serum COLEC10 levels are paradoxically elevated in patients with chr8 liver disease and serve as a biomarker for advanced fibrosis 56. These opposing expression patterns reflect COLEC10's dual roles: loss from hepatic stellate cells correlates with pathologic activation, while systemic elevation may reflect leakage during tissue remodeling.