This, along with our findings that hypercapnia downregulates MØ antiviral gene and protein expression (18) and that Zfh2 deficiency abrogates hypercapnic suppression of resistance to bacterial infection in Drosophila (19), led us to hypothesize that Zfhx3 might mediate the effects of elevated CO2 on lung MØs and host defense against IAV. Here, ZFHX2 is linked to bacterial infectious disease.