Due to developments in whole genome sequencing and elucidation of key signaling pathways, excessive IFN production and its associated interferon-stimulated gene expression signature is now an established molecular diagnostic of Mendelian inborn errors in immunity termed “interferonopathies.” In addition, identification of Mendelian loss-of-function mutations in critical mediators of the IFN response has been identified as the causal factors of immune deficiencies and susceptibility to viral infections. The gene discussed is IFNA1; the disease is viral infectious disease.