Because viral infection and upregulate IFN-β can induce IRF1 and IRF2 expression, when Type I Interferons signaling pathway is overactivated, IRF2, which acts as a transcriptional repressor through competing with IRF1 for binding to the IFNβ promoter region or Interferon-sensitive response element (ISRE) of the ISGs promoter subzone, negatively regulates IFNβ signal and interferon stimulated gene factor 3 (ISGF3)-mediated gene induction [9, 16–19]. Here, IFNB1 is linked to viral infectious disease.