Through the use of TGF-β1 ‘rescue’ experiments and β6 KO mice lacking type I IFN signaling, we were able to demonstrate the resistance of β6 KO mice to influenza depended on the loss of TGF-β1 and this elevated type I IFN signaling, while the phenotypic changes in lung macrophages were independent of the type I IFN pathway at least at the level of type I IFN signaling as shown in the β6/IFNAR double KO mice. The gene discussed is TGFB1; the disease is influenza.