Particularly, the constant augmentation of transcription factor NF-κB (nuclear factor kappa B; subunit RELA, inhibitor NFKBIB) and AP1 (activator protein 1; subunit FOS) expression during infection due to IRF7 deletion suggests that these factors complement IRF7 in the host antiviral response by modulating inflammatory cytokines and type I IFNs in chickens, as in mammals (Figure 5D, Figure S3) [52]. The gene discussed is FOS; the disease is infection.