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]. The gene discussed is NFKB1; the disease is Crohn disease.