The appearance of anti-IFN autoantibodies is correlated with age; they will increase the severity of the disease by delaying the prompt reaction of the immune system against the virus, which explains why patients with severe form of COVID-19 have a high percentage of autoantibodies targeting IFN, complement, interleukins, chemokines, and other immunomodulatory proteins, including those on the cell surface. This evidence concerns the gene IFNA1 and COVID-19.