Our previous studies showed that MCT4, an evaluated molecular and potential diagnostic marker in the intestinal mucosa of patients with inflammatory bowel disease, destroys intestinal barrier function by inhibition of cAMP-response element binding protein- (CREB-) mediated ZO-1 and activation of NF-κB-induced IL-6 expression [12, 13], indicating the critical role of the MCT4-mediated pathway in the development of IBD. This evidence concerns the gene TJP1 and inflammatory bowel disease.