GALNT14 (polypeptide N-acetylgalactosaminyltransferase 14) catalyzes the initial step of mucin-type O-linked oligosaccharide biosynthesis by transferring N-acetyl-D-galactosamine to serine or threonine residues on protein substrates, with particular activity toward mucin-derived peptides 1. The enzyme localizes to the Golgi apparatus and mediates protein O-glycosylation via N-acetyl-galactosamine 1. GALNT14 dysregulation contributes to multiple disease pathologies. In IgA nephropathy (IgAN), GALNT14 loss-of-function variants impair B lymphocyte homing and mucosal immunity rather than directly affecting IgA1 glycosylation, leading to aberrant IgA deposition and glomerular injury 12. In cancer, GALNT14 is frequently overexpressed and promotes progression through distinct mechanisms: in lung adenocarcinoma via ROS reduction through hnRNPUL1 O-glycosylation 3, in hepatocellular carcinoma via PHB2-Ser161 O-glycosylation activating IGF1R signaling 4, and in breast cancer via enhanced MMP-2 activity and epithelial-mesenchymal transition 5. GALNT14 expression also associates with stemness and drug resistance in breast cancer 6. Clinically, GALNT14 SNP rs9679162 genotypes predict therapeutic outcomes in hepatocellular carcinoma and gastrointestinal cancers 7, and GALNT14 inhibition with Bortezomib enhances chemosensitivity in osteosarcoma 8, positioning GALNT14 as a potential therapeutic target.