As a central transcriptional factor for induction of innate antiviral response, IRF3 needs to be fully activated in the early phase of viral infection, and then timely terminated to avoid excessive and harmful innate immune response.23,24 So far, various post-translational modifications, such as ubiquitination, sumoylation, and acetylation, have been reported to restrain IRF3 activity.25–27 In contrast, how IRF3 is optimally activated upon viral infection is not fully understood. Here, IRF3 is linked to viral infectious disease.