In our pervious study, MCT4, a chaperone of CD147, has been reported to increase in the intestinal mucosa in IBD [12], and alterations of MCT4 expression are sufficient to induce a switch between CBP-NF-κB and CBP-CREB complex, leading to different biological functions in inflammatory bowel disease, and treatment of experimental colitis with MCT4 inhibitor α-cyano-4-hydroxycinnamate (CHC) ameliorated mucosal intestinal barrier function, which was due to attenuation of proinflammation factor expression and enhancement of ZO-1 expression [12, 13]. Here, TJP1 is linked to inflammatory bowel disease.