These results showed that the deletion of RIPK3, but not the MLKL deficiency or RIPK1 kinase‐dead mutation, could rescue Abin1Q478H/Q478H mice from anemia, suggesting that RIPK3 promotes anemia in Abin1Q478H/Q478H mice through necroptosis‐independent functions. The gene discussed is MLKL; the disease is anemia (phenotype).