Although it is possible that cooperative combinations of several IFNs (IFNα/β, IFNγ, IFNλ) that signal through STAT1 are required to regulate SARS-CoV infection, we feel that the possibility exists that STAT1's role in controlling cell proliferation and wound healing may be the base cause of the increased disease seen in STAT1−/− mice. The gene discussed is IFNG; the disease is severe acute respiratory syndrome.