Dahan et al. (2011) found that the absence of the Notch-1 signaling pathway markedly upregulated claudin-2 and downregulated occluding, and N1ICD is increased in patients with inflammatory bowel disease. Ahmed et al. (2018) showed the dysfunction of ZO-2, β-catenin, and E-cadherin in Notch suppression by dibenzazepine, which further resulted in increased permeability of epithelial cells in infectious colitis. Here, CLDN2 is linked to inflammatory bowel disease.