However, interferon-stimulated genes (ISGs) with antiviral function were similarly upregulated on infection with the X31 virus strain in primary airway epithelia from 129 and IFNαβR−/−(129) mice (Fig. 4a), consistent with the suggested redundancy of IFNαβ and IFNλ in epithelial cells29, 30. The gene discussed is IFNAR2; the disease is infection.