Some key elements of NFκB-IRF pathway cross-talk are that: (1) the virus infection-activated IFNβ enhanceosome is activated by NFκB (note that IFNβ is a major type I IFN, responsible for the majority of mucosal anti-viral effect); (2) the induction of inducible IRF-1 and -7 subunits controlling type I IFN expression are dependent on direct NFκB transactivation [33]; and, (3) NFκB is required for the IRF-IFN-RIG-I amplification loop, described above [34]. This evidence concerns the gene TRIM63 and viral infectious disease.