RLRs bind to MAVS upon virus infection and activate TBK1 and IκB kinase ε (IKKε), leading to the induction of IRF3 and IRF7, which together with the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) promote the expression of IFN-I, and large quantities of cytokines participated in antiviral innate immunity (Rehwinkel and Gack, 2020). This evidence concerns the gene IRF3 and viral infectious disease.