By altering the ratio of the IKKs, the virus could affect the canonical versus noncanonical pathways or could create differing combinations of possible dimeric IKKs that in either case could potentially favor the types of NF-κB family members produced during infection, which in turn would allow selective regulation of only those NF-κB-dependent promoters that favor viral infection and persistence. Here, NFKB1 is linked to infection.