In particular, Williams et al. (8) observed that Casp11−/− mice displayed a significantly increased morbidity, colonic tissue damage, and leukocyte infiltration following DSS exposure, thus suggesting an increased susceptibility to DSS-induced colitis that was ascribed to a decrease in colonic inflammasome-induced IL-1β and IL-18 release (8). The gene discussed is IL18; the disease is colitis.