The expression and function of the anion exchanger pendrin (SLC26A4) was thought to be limited mainly to the inner ear, kidney and thyroid. Recent data indicates that pendrin is also expressed in the bronchial epithelium following exposure to the T_H2-type cytokines, interleukin (IL)-4 and IL-13. Expression of the transporter is also upregulated in bronchial asthma and chronic obstructive pulmonary disease. Both diseases involve respiratory inflammation leading to tissue destruction/remodeling and decreased airway function, and data so far indicate that increased pendrin expression and/or activity might contribute to their pathogenesis. In this review, we summarize data that have emerged within the past years aimed at revealing the role for pendrin in the airway epithelia.