Consistent with the above results, Zaki et al. observed that the induction of colitis in Nlrp3−/− mice was associated with a disruption of intestinal epithelial barrier and an increase in mucosal permeability as compared to DSS wild-type (WT) mice, with consequent bacterial translocation into the mucosa and systemic dissemination (37). The gene discussed is NLRP3; the disease is colitis.