However, Ifnar1–/– mice have been shown to prevent HSC exhaustion resulting from chronic stimulation with type I IFNs.[7] To further investigate whether Abin1Q478H/Q478H mice develop hematopoietic diseases as a result of the excessive activation of type I IFN signaling, we crossed Ifnar1‐knockout mice with Abin1Q478H/Q478H mice. This evidence concerns the gene IFNAR1 and hematologic disorder.