Interestingly, IL-1β, one of the products of pyroptosis, has been reported to be an important mediator of inflammation and tissue damage in IBD, and IL-1β induced defects in intestinal epithelial tight junctions resulting in increased intestinal permeability [15], while IL-18 has been also shown to contribute to the breakdown of the mucosal barrier, triggering inflammation and amplifying damage elicited to the intestinal epithelium during disease [16]. This evidence concerns the gene IL18 and inflammatory bowel disease.