NFKB1 and viral infectious disease: A variety of stimuli can activate the NF-κB response, such as cytokine stimuli (Tumor Necrosis Factor –α [TNF-α], Interleukin-1 [IL-1]), UV stress, DNA damage, lipopolysaccharide and virus infection, which result in p65 nuclear translocation and transcription regulation [12], [13], [15]–[21].