Early studies employing mutant mice confirmed that activated caspase-1 was crucial for DSS-induced inflammation, as mice deficient in caspases-1 or NLRP3 experienced significantly less severe pathology than wild-type (WT) mice, which was correlated with reduced levels of IL-1β and IL-18, indicating that excessive production of IL-18 could aggravate the DSS induced colitis (90–92). The gene discussed is IL18; the disease is colitis.