It is well known that caspase-1 mediates pyroptosis when activated by the canonical inflammasome NLRP3, interacts with the adaptor protein ASC in response to microbial infection after the intestinal epithelial barrier disruption, and then cleaves the pyroptosis effector GSDMD, releasing pro-inflammatory mediators mature IL-18 and HMGB1 to the outside of cells, which is associated with the pathogenesis of Crohn’s disease (Villani et al., 2009; Zaki et al., 2010). This evidence concerns the gene NLRP3 and Crohn disease.