FUT1 encodes fucosyltransferase 1, a Golgi membrane enzyme that catalyzes the transfer of L-fucose to terminal galactose residues through α(1,2) linkage, essential for H antigen synthesis and ABO blood group antigen formation 1. Beyond blood group determination, FUT1 plays critical roles in cancer biology and immune regulation. In hepatocellular carcinoma, glucose deprivation upregulates FUT1 through PERK/eIF2α/ATF4 signaling, promoting cancer stemness by fucosylating key glycoproteins including CD147, ICAM-1, EGFR, and EPHA2, which converge on AKT/mTOR/4EBP1 pathways to drive tumor initiation, self-renewal, and drug resistance 2. Pan-cancer analysis reveals FUT1 overexpression correlates with poor prognosis in multiple cancer types and associates with proliferation, metastasis, and epithelial-mesenchymal transition pathways 3. FUT1 also regulates immune function, as its deficiency causes immune dysregulation and corneal opacity through enhanced Th1 cell activation and inflammatory responses 4. In allergic rhinitis, FUT1 downregulation improves dendritic cell IL-10 metabolism and suppresses Th2 differentiation through the FUT1/ICAM1/P38 MAPK pathway 5. Clinically, FUT1 mutations cause rare Bombay and para-Bombay blood phenotypes, creating transfusion challenges due to anti-H antibodies 6.