Given the prevalence of UPEC‐mediated UTI, the abundance of UP on the urothelium and the requirement of FimH‐mediated UPEC adhesion to initiate UTI, binding of FimH to mannose groups of UP1a exemplifies a key glycan target to disrupt host–pathogen interactions (Figure 1a). The gene discussed is UPK1A; the disease is bacterial urinary tract infection.