As NFκB1 is a nexus point for multiple redundant inflammatory mediators to start the innate immune response, and genetic variations such as SNPs can contribute to higher levels of transcription, production, and activity of inflammatory as well as anti-inflammatory cytokines, it is hypothesized that individual polymorphic NFκB1 variations could be responsible for the cytokine upregulation, leading to the severe disease response that were seen during the influenza H1N1 pandemic [31,32]. This evidence concerns the gene NFKB1 and influenza.