Furthermore, in a seminal study describing a protective role for IL-33 in colitis, Malik et al. demonstrated that Il33−/− mice were more susceptible to DSS-induced tissue damage and colitis-associated tumorigenesis, phenotypes which were both due to elevated concentrations of IL-1α in the absence of IL-33 and which could be ameliorated via abolition of IL-1α signaling (160). The gene discussed is IL1A; the disease is colitis.