Given that many respiratory viruses cocirculating with SARS-CoV-2 (such as influenza virus, rhinovirus, or seasonal coronaviruses) can trigger host IFN production, as well as the recent repurposing of IFNs in clinical trials as COVID-19 therapeutics (16), we sought to understand the interplay between the antiviral action of IFNs (17), the IFN-stimulated expression of ACE2 (9, 12, 13), and SARS-CoV-2 replication. The gene discussed is ACE2; the disease is COVID-19.