Together with our prior findings demonstrating that CFTR modulation reduces epithelial release of the potent type 2 cytokine IL-33 and our present studies showing significant GATA3 and IL-13 reductions in human Th2 cells treated with ivacaftor compared with DMSO controls, CFTR modulation has the potential to broadly target allergic disease. The gene discussed is CFTR; the disease is allergic disease.