CLDN7 and colitis: Abnormal expression of Claudin can lead to reduced adhesion, structural damage, and impaired function of epithelial and endothelial cells.[66] Importantly, inducible intestinal Cldn7 knockout could cause disruption of the intestinal mucosal barrier in mice.[67] Intestinal epithelial-specific knockdown of Cldn-7 increases susceptibility to DSS-induced colitis.[68] In addition, mice developed histopathological features of CD at 3 months of age due to endogenous E-calcineurin deficiency.[3] Collectively, disruption of intestinal barrier exacerbates intestinal inflammation.