SLC26A9 and cystic fibrosis: Such interest arises from various preliminary observations: (1) it was originally described as a protein expressed in the lung [18]; (2) given the family it belongs to, it presumably mediates anion transport activity; (3) SLC26A9-deficient mice exposed to inflammatory stimuli exhibited a CF-like lung phenotype characterized by airway mucus obstruction [19]; (4) it has already been investigated as a modifier of the phenotype and therapeutic response of CF patients [20,21,22,23].