GAL3ST1 encodes galactose-3-O-sulfotransferase 1, which catalyzes sulfation of non-reducing terminal galactose residues on glycerolipids and sphingolipids, producing sulfatides and related sulfoglycolipids. The enzyme is essential for synthesis of galactosylceramide sulfate (sulfatide), a major myelin component, and seminolipid in spermatocytes. GAL3ST1 is implicated in diverse pathogenic contexts: biallelic mutations cause autosomal recessive spinocerebellar ataxia 16 and adult-onset cerebellar ataxia; genome-wide association studies identify GAL3ST1 variants as risk loci for sporadic Creutzfeldt-Jakob disease, where reduced sulfatide levels are linked to impaired protection against prion misfolding 12. In cancer, GAL3ST1 overexpression is observed in clear cell renal cell carcinoma, cholangiocarcinoma, and pancreatic intraductal papillary mucinous neoplasms; elevated sulfatide enhances immune evasion via increased tumor cell–platelet binding and supports metabolic vulnerabilities exploitable by targeting upstream enzymes 34. Recent work demonstrates that GAL3ST1 upregulation via FOXA1 transcription factor activation mediates growth inhibition in obesity-associated triple-negative breast cancer following astragaloside IV treatment 5. Additionally, sulfatide–selectin interaction in the spinal cord contributes to inflammatory pain 6, and dysregulated sulfatide metabolism correlates with Alzheimer's disease pathology 7.