To test this hypothesis, we aimed to (a) assess T cell–specific CFTR loss in in vitro and in vivo models of allergic airway inflammation, (b) determine the molecular pathways underlying increased CD4+ T cell effector function in response to CFTR functional loss, and (c) test for the therapeutic benefit of CFTR potentiation in Th2-mediated allergic disease. This evidence concerns the gene CD4 and allergic disease.