Since this first description was based on targeting of p40 and therefore suppressing IL-12 and IL-23 action, the contribution of each of those cytokines is still not completely understood in human disease, but in TNBS colitis, suppressing IL-23 unleashes IL-12 production via IL-17A and T-bet and therefore exacerbates colitis; so in this model, Th1 action seems to dominate [102, 103]. This evidence concerns the gene IL17A and colitis.