In general, the initial activation of the antiviral innate immune response to viral infections primarily depends on the expression of antiviral cytokines, such as type I and III IFNs, which are produced by various cells [35,36,37] through the activation of downstream transcription factors, such as IRFs and NF-kB, via MyD88-dependent and -independent immune signaling pathways [38]. This evidence concerns the gene NFKB1 and viral infectious disease.