GALNT9 (polypeptide N-acetylgalactosaminyltransferase 9) catalyzes the initial step of mucin-type O-linked glycosylation by transferring N-acetyl-D-galactosamine to serine or threonine residues on protein substrates 1. This Golgi-localized enzyme mediates the addition of O-GalNAc glycans to cell surface proteins, including adhesion molecules like Annexin A2 2. GALNT9 plays critical roles in disease pathogenesis across multiple contexts. In neuroendocrine cancers, aberrantly elevated GALNT9 expression drives liver-specific metastasis by decorating cancer cell surfaces with O-GalNAc glycans that activate mannose-binding lectin complement signaling, triggering platelet activation and thrombus formation 2. Conversely, GALNT9 deficiency contributes to Parkinson's disease pathogenesis by reducing dopamine levels and promoting α-synuclein aggregation through impaired glycosylation of mitochondrial proteins (ACO2, ATP5B, CKB, CKMT1A, ALDOC), leading to mitochondrial dysfunction, ROS accumulation, and apoptosis 13. GALNT9 expression serves as a favorable prognostic marker in neuroblastoma, correlating with improved overall and disease-free survival 4. Additionally, GALNT9 methylation in circulating cell-free DNA shows promise as a noninvasive biomarker for colorectal cancer screening 5, and rare variants in GALNT9 are associated with papillary thyroid carcinoma risk 6. GALNT9 loss-of-function variants also link to late-onset corneal dystrophies in aging populations 7.