To pursue this aim, the experiments were performed in a rat model of DNBS-induced colitis, resembling human Crohn’s disease in terms of macroscopical (bodyweight loss, diarrhea, ulceration, and bleeding), histological, and immunological features including depletion of goblet cells and transmural infiltration of polymorphonuclear cells and predominant NF-κB-dependent Th1 activation [46]. This evidence concerns the gene NFKB1 and colitis.