These data suggest that pendrin promotes Cl−/HCO3− transport during inflammation (Haggie et al., 2016; Kim et al., 2019; Rehman et al., 2020), but whether functional interplay between CFTR and pendrin (Rehman et al., 2020; Tamma and Dossena, 2022) is defective in CF airway leading to loss of HCO3− secretion remains to be explored in future work. This evidence concerns the gene SLC26A4 and cystic fibrosis.