It was reported that NLRP3 may confer protection against colitis and colitis-associated tumorigenesis, by mediating the secretion of IL-18, which could promote intestinal epithelial cell differentiation, maintain intestinal epithelial integrity, and reduce intestinal epithelial cell proliferation during colitis remission; NLRP3 deficient mice were found to be more susceptible to dextran sodium sulfate (DSS) and 2,4,6-trinitrobenzenesulfonic acid, and showed more sever colonic inflammation, and higher carcinogenesis (Allen et al., 2010; Zaki et al., 2010; Zaki et al., 2011). This evidence concerns the gene IL18 and colitis.