In recent years, our understanding of the importance of intestinal barrier function and epithelial TJ alterations for the pathogenesis of barrier disorders considerably increased, e.g., with a reduced expression of occludin and claudin-4 in collagenous colitis [29], and of claudin-5 and claudin-8 in Crohn’s disease, as well as an increase in the channel-forming TJ protein claudin-2 in ulcerative colitis [30]. This evidence concerns the gene CLDN2 and Crohn disease.