By using two experimental mouse models of chemical induced IBD, triggered either by dextran sodium sulphate (DSS) or by 2,4,6-trinitrobenzene sulphonic acid (TNBS), Sedhom and colleagues showed that injection of IL-33 could accelerate colitis, and the disease induction could be effectively prevented by blocking the IL-33-ST2 axis either through genetic ablation of the ST2 gene or the use of neutralizing antibodies [45]. The gene discussed is IL1RL1; the disease is inflammatory bowel disease.