Ultimately, activation of MAVS or STING results in nuclear translocation of interferon regulatory factor 3 (IRF3) and IRF7, which together with the transcription factor nuclear factor-κB (NF-κB) drive the production of type I interferons (IFNs) that induce expression of antiviral IFN-stimulated genes (ISGs) to restrict viral infection in an autocrine and paracrine manner (Rehwinkel and Gack, 2020). This evidence concerns the gene IRF3 and viral infectious disease.