Up to this point, our analyses indicate specialized IFN action in the context of SARS-CoV-2 infection, which could be explained by several nonmutually exclusive potential mechanisms, including tissue-specific expression of IFNs (22), variable timing of IFN production during the course of viral infection (23), self-amplification of certain IFNs via positive feedback (24, 25), differential turnover of IFNs in circulation (26), or blockade of specific IFN subtype production by SARS-CoV-2 proteins (27). Here, IFNA1 is linked to viral infectious disease.