showed that aged macaques have a stronger host response to virus infection compared to young macaques, with an increase in differential expression of genes associated with inflammation, with NF-κB as central player, whereas expression of type I interferon was reduced indicating a possible negative-feedback cross-talk between the pro-inflammatory NF-κB pathway and IFN-induced antiviral pathways (26). Here, NFKB1 is linked to viral infectious disease.