For example, while in vitro evidence suggests that NLRP3 inflammasome and IL-1β activation in the absence of A20 (encoded by TNFAIP3) is regulated by RIPK3-caspase-8 signalling, a recent study in A20LysM.cre mice showed that loss of RIPK3, MLKL, or the kinase activity of RIPK1, dampened IL-1β activity and alleviated arthritis symptoms [130]. This evidence concerns the gene CASP8 and arthritic joint disease.