CFTR and cystic fibrosis: Here, we demonstrate that ASO-ψ, an ASO designed to block splicing to the aberrant ψ-Ex splice site created by the CFTR c.3718-2477C>T mutation, redirects splicing to the correct, wild-type splice site, increases forskolin-stimulated apical membrane conductance and restores chloride secretion in CF patient-derived bronchial epithelial cells.