However, other authors did not show a negative regulatory effect of NLRP3 on colitis, showing that NLRP3-null mice or mice pretreated with the caspase-1 inhibitor pralnacasan had less severe colitis when treated with DSS, which was related to decreased IL-1β secretion of DSS-exposed NLRP3-deficient macrophages in vitro [52, 53]. The gene discussed is NLRP3; the disease is colitis.