The implications of these findings are that (i) a defective SCN− secretion via pendrin might be linked to increased bacterial colonization of the airway epithelium147 and (ii) inhibition of pendrin activity150 or peroxidase‐dependent conversion of SCN− to OSCN−151 might be beneficial in treating asthma and other chronic inflammatory airway conditions. This evidence concerns the gene SLC26A4 and asthma.