Although one of the first observations of IL-33-dependent functions in the gut was potent epithelial proliferation and mucus production (26), suggesting the promotion of mucosal repair and healing, dysregulated or uncontrolled IL-33 production may also lead to more pathogenic features characteristic of IBD, including epithelial barrier dysfunction, chronic, relapsing inflammation, and formation of fibrotic lesions (27, 28). This evidence concerns the gene IL33 and inflammatory bowel disease.