This puts into questions whether the unresponsiveness of the Casp8−/−; Mlkl−/− mice to SIRS (C57BI/6N) is solely due to loss of apoptosis or both, apoptosis and necroptosis and, most importantly, whether RIPK3 might play a role in inflammation independently of MLKL also in this pathological context. This evidence concerns the gene RIPK3 and systemic inflammatory response syndrome.