Although earlier studies in the collagen- and antigen-induced arthritis models suggest that disease pathology is ASC-related but independent of NLRP3 [11, 12], more recent studies in a novel spontaneous arthritis model (A20myel-KO mice) show that arthritis pathology critically relies on the NLRP3 inflammasome/IL-1β axis [13]. The gene discussed is IL1B; the disease is arthritic joint disease.