NLRP3-mediated inflammasome assembly has been demonstrated to be important in both human and mouse models of IBD,23 and similarly it is known that the NLRP7 protein can promote both positive and negative regulation of inflammasome activity.24 For example, it is required for bacterial acylated lipoprotein-mediated caspase-1 activation and maturation of IL-1β and IL-18, but has also been shown to inhibit NLRP3 and caspase-1-mediated IL-1β release. This evidence concerns the gene NLRP3 and inflammatory bowel disease.