Other independent groups replicated similar results, using the same acute animal model [63–65]; in addition, Sedhom et al. confirmed the pathogenic role of IL-33 also in a different model of intestinal inflammation, the trinitrobenzene-sulfonic-acid- (TNBS-) induced colitis, which is obtained throughout the chemical haptenization of protein expressed within the gut wall [64]. This evidence concerns the gene IL33 and colitis.