The study investigates the role of caspase-8 (Casp8) and RIP3 in embryonic development and immune homeostasis. Casp8 is crucial for death receptor-induced apoptosis and non-apoptotic pathways, while RIP3 is involved in necroptosis. Disruption of *Casp8* expression leads to embryonic lethality between E10.5 and E11.5, with defects in vascular, cardiac, and hematopoietic systems. However, *Casp8*^−/−^*Rip3*^−/−^ double mutant mice are viable and mature into fertile adults, but develop lymphadenopathy by four months of age, characterized by the accumulation of abnormal T cells, similar to *lpr/lpr* mice. The data suggest that Casp8 suppresses RIP3-dependent necroptosis during embryogenesis, and its absence leads to the accumulation of abnormal T cells, contributing to lymphadenopathy and splenomegaly. The findings highlight the importance of Casp8 in controlling RIP3 pathways and maintaining immune homeostasis.The study investigates the role of caspase-8 (Casp8) and RIP3 in embryonic development and immune homeostasis. Casp8 is crucial for death receptor-induced apoptosis and non-apoptotic pathways, while RIP3 is involved in necroptosis. Disruption of *Casp8* expression leads to embryonic lethality between E10.5 and E11.5, with defects in vascular, cardiac, and hematopoietic systems. However, *Casp8*^−/−^*Rip3*^−/−^ double mutant mice are viable and mature into fertile adults, but develop lymphadenopathy by four months of age, characterized by the accumulation of abnormal T cells, similar to *lpr/lpr* mice. The data suggest that Casp8 suppresses RIP3-dependent necroptosis during embryogenesis, and its absence leads to the accumulation of abnormal T cells, contributing to lymphadenopathy and splenomegaly. The findings highlight the importance of Casp8 in controlling RIP3 pathways and maintaining immune homeostasis.