While the up-regulation of IFNs promotes the resolution of viral infections, prolonged or excessive activation of the immune response after viral infection or aberrant activation of IFN signaling by endogenous RNAs can lead to sustained production of pro-inflammatory cytokines, which can be a risk factor for inflammatory diseases such as atherosclerosis, rheumatoid arthritis, multiple sclerosis, asthma, and COPD [12,17–19]. The gene discussed is IFNA1; the disease is viral infectious disease.