Furthermore, a reduction in a specific biochemical fraction of colonic mucin has been described in UC patients and in their unaffected monozygotic twins [18,19], and engineered changes in intestinal mucin glycosylation result in enhanced susceptibility to toxin-induced colitis [20], raising the possibility that genetic defects in mucin physiology or biochemistry predispose to UC. This evidence concerns the gene MUC5AC and colitis.