Concerning the site of action of B14, it is clear that B14 shuts down expression of reporter genes with NF-κB-responsive promoters in response to multiple stimuli (Figure 1) and that within infected cells the overall level of IκBα is not altered by virus infection (Figure 5) or by the expression of B14 in resting cells (Figure 4). Here, NFKBIA is linked to viral infectious disease.