After viral infection, IκB kinase-epsilon (IKKε) and TANK-binding kinase 1 (TBK1), two homologs of the inhibitor of NF-κB kinase (IKK), are activated when PRRs convey the sensing of virus infection to their adaptor proteins, inducing conformational changes and interactions that lead to the formation of a new interaction surface (reviewed in [13]). This evidence concerns the gene IKBKE and viral infectious disease.