In addition to evidence supporting weak and shortened levels of IFNα by SARS-CoV-2 infection in critically ill COVID-19 patients, molecular data have started to document the capacity of SARS-CoV-2 to evade the IFN response as previously documented for SARS-CoV (Lei et al., 2020b; Park and Iwasaki, 2020; Xia et al., 2020b). The gene discussed is IFNA2; the disease is COVID-19.