In particular, NLRP3 inflammasome-induced IL-1β and IL-18 release from monocytes infiltrating the lamina propria alters tight junctions and promotes apoptosis in intestinal epithelial cells, and, subsequently M1 macrophages, recruited into the lamina propria, contribute to sustain the immune innate response, thus suggesting a detrimental role of NLRP3 inflammasome in IBD patients (76). This evidence concerns the gene IL18 and inflammatory bowel disease.