SLC35A3 is a Golgi membrane transporter that mediates UDP-N-acetylglucosamine (UDP-GlcNAc) transport from the cytosol into the Golgi lumen, functioning as an antiporter that exchanges UDP-GlcNAc for UMP 1. The transporter supplies UDP-GlcNAc as substrate for glycosyltransferases generating complex N-glycans and keratan sulfate 23. However, SLC35A3's precise role remains incompletely understood; it may function as part of a multiprotein complex rather than independently 4. Recent evidence suggests SLC35A3 cooperates with the homologous SLC35A2 protein to restore proper glycosylation, and its O-GlcNAcylation by OGT specifically regulates branched N-glycan biosynthesis via interaction with GnT-IV 53. Mutations in SLC35A3 cause congenital disorders of glycosylation (CDG) characterized by skeletal dysplasia, vertebral anomalies, cleft palate, and neurological features including autism, epilepsy, and arthrogryposis 6. Clinically, decreased SLC35A3 expression in colorectal cancer associates with poor prognosis, increased immune infiltration, and reduced survival outcomes, suggesting SLC35A3 serves as an independent prognostic biomarker 7. SLC35A3 also functions in glycolysis-related prognostic models for gastric cancer 8. These findings establish SLC35A3's dual importance in normal glycosylation homeostasis and cancer progression.