For example, it is established that Helicobacter pylori binds to histo-blood group antigens H-type-1 structures and Leb antigens via its group antigen-binding adhesin (BabA).84 Studies in Fut2-/- mice, as well as in humans who are nonsecretors as discussed above (i.e., loss of function alleles in FUT2), reveals the loss Blood Group A on gastric mucins renders tissues refractory to infection by BabA+ strains,161,162 highlighting a role in pathogenesis. Here, FUT2 is linked to infection.