Upon virus infection, IRF3 is phosphorylated by the kinases TBK1 and IKKε at its C-terminus, forming dimers that are then transported into the nucleus (Honda and Taniguchi, 2006; Zhao et al., 2007), subsequently forming a complex with the coactivators of the p300/CBP family and initiating transcription of target genes, including IFN-β (Servant et al., 2003; Takahasi et al., 2010). Here, IRF3 is linked to viral infectious disease.