Its upregulation aggravated the experimental colitis via the inhibition of aryl hydrocarbon receptor (AHR), which is proved to be responsible for the lowering of proinflammatory cytokines (IL-6, IL-7, IL-12, IL-17, TNF, and IFN Y), reduction of microbial translocation and development of fibrosis in the colon [99,100,101,102]. This evidence concerns the gene TNF and colitis.