Due to the discrepancy between the lower iodide transport activity of SLC26A7 and the clinical severity of thyroid dysfunction in patients with a mutation in SLC26A7 compared to those with Pendred syndrome, we speculate that SLC26A7 may be expressed more abundantly than SLC26A4 in the human thyroid gland or that SLC26A7 may have another function in addition to being an iodide transporter. Here, SLC26A7 is linked to Pendred syndrome.