IRF3 and viral infectious disease: Previous studies have shown that an IRF7 mutant, IRF7m, lacking the amino acid residues from 284 to 454, a region that includes the auto-inhibitory domain (from amino acid residue 305 to 467), and an IRF3 mutant, IRF3m, carrying the substitution of Ser396 to Asp in the carboxyl terminal region (Fig. 1A), induced a potent activation of type I IFN promoter in non-hepatic cell lines irrespective of viral infection [22]–[25].