CFTR and cystic fibrosis: Initial studies have shown that Slc26a9 contributes to constitutive and cyclic adenosine monophosphate (cAMP)-dependent Cl- secretion in cultured human bronchial epithelial (HBE) cells, and Slc26a9 has been suggested to functionally interact with CFTR in vitro (Bertrand et al., 2009; Avella et al., 2011), indicating that Slc26a9 may serve as a chloride channel that compensates for CFTR dysfunction in CF.