A previous study suggested that the UBD of ABIN1 was important for controlling the TNF signaling and TLR–MyD88 pathways.[9, 10, 11] In this study, we found that Abin1Q478H/Q478H knock‐in mice developed spontaneous anemia and thrombocytopenia through excessive activation of TRAF3‐regulated type I IFN signaling. The gene discussed is TNF; the disease is anemia (phenotype).