In a broad sense, the data suggest that the role and regulation of NF-κB are likely more complex than appreciated and that the virus takes advantage of these complexities and utilizes the positive aspects of NF-κB signaling to support lytic and latent infection while mitigating the negative aspects of the NF-κB-induced immune response. This evidence concerns the gene NFKB1 and disease arising from reactivation of latent virus.