SLC35C1 is a GDP-fucose antiporter that mediates the transport of GDP-L-fucose into the Golgi lumen while returning GMP to the cytoplasm 1. This transporter is essential for protein fucosylation, a critical post-translational modification that affects glycan-dependent cellular functions 2. Mechanistically, SLC35C1 facilitates the fucosylation of adhesion molecules and other glycoproteins required for proper immune cell function and cell-cell interactions 3. In cholestatic liver disease, elevated hepatic SLC35C1 expression is induced by bile acid-stimulated STAT3 signaling, where it enhances CEACAM1 fucosylation at N153 to suppress inflammatory chemokine (CCL2, CXCL2) expression and attenuate liver injury 1. Mutations in SLC35C1 cause leukocyte adhesion deficiency type II (LAD II), a congenital disorder of glycosylation characterized by immunodeficiency, growth impairment, and recurrent infections 3. Oral L-fucose supplementation can improve immune function and cognition in patients with milder variants 3. Beyond immune dysfunction, SLC35C1 expression correlates with tumor microenvironment composition, immune infiltration, and prognosis across multiple cancer types, with experimental evidence suggesting roles in glioma cell proliferation and migration 4. Clinically, SLC35C1-CDG is one of the few CDG types with available targeted therapy, making it a therapeutic priority among glycosylation disorders 56.