In support of the above results, showing a detrimental role of NLRP3 in bowel inflammation, Zhang et al. (9) observed a causative link between NLRP3 inflammasome activation and development of chronic intestinal inflammation, showing that the increase in colonic IL-1β levels in IL-10−/− mice promoted IL-17 release, known to contribute to the pathogenesis of chronic colitis both in animal models and IBD patients (42). The gene discussed is NLRP3; the disease is inflammatory bowel disease.