Many viruses, including SARS-CoV-2, have evolved escape mechanisms against the antiviral activity of IFN-I.28 Recent studies had shown that although the production of TNF and IL-6 was increased, and the NF-κB-driving inflammatory response was highly activated, the IFN-I response in seriously ill COVID-19 patients and rhesus monkeys infected with SARS-CoV-2 were still impaired.9,29 These findings indicated that IFN-I should be treated as a target for the treatment of COVID-19. Here, TNF is linked to COVID-19.