It has been previously demonstrated that the two non-canonical IκB kinase homologs, namely IκB kinase-ε (IKK-ε or IKKi) and TANK-binding kinase-1 (TBK1), are involved in the C-terminal phosphorylation of IRF3 upon dsRNA stimulation or viral infection [15], [16]. This evidence concerns the gene IRF3 and viral infectious disease.