FUCA1 and common variable immunodeficiency: A multifactorial genesis likely underlies the hyperfucosylation observed in CD21low B cells, as the upregulation of FUT7, FUT8, FUCA1, FUCA2, and FUOM in naïve-like CD21low B cells from CVID patients suggests the relevance of fucosyltransferases and their substrate availability, potentially stemming from increased recycling of fucose (48, 49).