SLC26A9 and cystic fibrosis: This current was absent from HBE cells cultured at air liquid interface (ALI) from CF patients, and furthermore, these cells lacked the signature currents, typical of SLC26A9 alone or coexpressed with WT-CFTR in HEK 293 coexpressing F508del-CFTR and SLC26A9 [53], suggesting that the mutant CFTR prevented SLC26A9 activity.