When embryonic lethality in Casp8-deficient mice is rescued by Ripk3 or Mlkl ablation, the Casp8−/−Ripk3−/− and Casp8−/−Mlkl−/− mice develop lymphadenopathy [11] that resembles the abnormality observed in Fas ligand (FasL, CD95L) [28] or FAS [29, 30] deficient mice and human autoimmune lymphoproliferative syndrome (ALPS) [31, 32]. This evidence concerns the gene FAS and autoimmune lymphoproliferative syndrome.