Based on limited published evidence, FUOM (fucose mutarotase) catalyzes interconversion between alpha- and beta-L-fucoses, enabling L-fucose salvage pathway metabolism. The enzyme converts L-fucose to GDP-L-fucose for transport into the endoplasmic reticulum, where it serves as substrate for fucosyltransferases mediating N- and O-glycosylations. Fucosylated glycans play critical roles in cell-cell adhesion and recognition. Recent studies identify FUOM as a potential driver in cervical cancer, where FUOM knockdown reduced cell proliferation (37%), migration (43%), and colony formation (62%) 1, and as a causal plasma protein in hepatocellular carcinoma 2.