In other SARS-COV infections, the virus can evade the IFN signaling both at the stage of IFN induction via ubiquitination and degradation of the RNA sensor adaptor molecules or via inhibiting IRF3 nuclear translocation, as well as at the stage of IFN secretion, by decreasing STAT1 phosphorylation [67–69]. The gene discussed is IFNA1; the disease is severe acute respiratory syndrome.