These include a host antiviral response to SARS-CoV-2 in nasal epithelial cells that is dominated by IFN signaling [8], repression of in vitro SARS-CoV-2 replication by type I IFN [9,10], and poor viral replication and less severe COVID-19 symptoms in individuals with a robust IFN-induced antiviral response in the early phase of infection [11,12]. The gene discussed is IFNA1; the disease is infection.