Our study of gene expression responses by CF AECs exposed to ETI suggests that in addition to improving CFTR channel function, ETI is likely to increase resistance to bacterial infection, and thereby account for the modest reduction in lung bacteria by increasing hBD-1, reducing lung damage by suppressing MMP10, and decreasing inflammation by repressing proinflammatory cytokine secretion. The gene discussed is DEFB1; the disease is cystic fibrosis.