GALNT7 is a glycosyltransferase that catalyzes O-linked oligosaccharide biosynthesis by transferring N-acetylgalactosamine residues to glycosylated peptides in the Golgi apparatus. Unlike other family members, GALNT7 primarily acts on already-glycosylated substrates rather than initiating glycosylation de novo, though some peptide transferase activity cannot be excluded. GALNT7 has emerged as a significant oncogenic driver across multiple cancer types. In prostate cancer, GALNT7 is upregulated and promotes tumor growth through altered O-glycosylation patterns, with diagnostic utility in urine and blood samples superior to PSA alone 1. In hepatocellular carcinoma, GALNT7 drives progression via O-glycosylation of MUC13, activating the PI3K/AKT signaling pathway and conferring lenvatinib resistance 2. GALNT7 overexpression similarly promotes cervical cancer and nasopharyngeal carcinoma cell proliferation and invasion 3 4. In glioma, GALNT7 participates in tumorigenesis through a competing endogenous RNA mechanism involving TP73-AS1 and miR-103a 5. In dMMR/MSI colorectal cancers specifically, high GALNT7 expression associates with favorable prognosis and reduced PD-L1 expression, distinguishing this cancer subtype from microsatellite-stable disease 6. Beyond malignancy, GALNT7 participates in doxorubicin cardiotoxicity through the miR-30d-5p axis, with exercise-induced GALNT7 upregulation conferring cardioprotection 7. These findings position GALNT7 as both a therapeutic target and biomarker across disease contexts.