We observed that global deletion of RIPK3 in both of our caspase-8 deletion constructs (CreLysMCasp8flox/flox and CreCD11cCasp8flox/flox) caused the response to K/BxN serum-transfer-induced arthritis to revert back to that of control Casp8flox/flox mice, potentially independent of controlling necroptosis. This evidence concerns the gene CASP8 and arthritic joint disease.