Further, a recent longitudinal analysis illustrated that IFN-α levels in peripheral blood remained high in patients with severe COVID-19 and that classical monocytes exhibit both IFN-I and TNF/IL-1β-driven inflammatory responses (94), and approximately 10% of patients with severe COVID-19 had neutralizing immunoglobulin (Ig)G auto-antibodies against type I IFNs (248, 249); hence these patients required plasma exchange (250). Here, IFNA2 is linked to COVID-19.