A significant proportion of patients with aggressive thyroid cancer fail to respond to radioiodide (RAI) therapy, the systemic treatment of choice for metastatic disease, and no effective alternative treatment exists. In other tumors, such as breast cancers, where the possibility of using RAI as a coadjuvant/neoadjuvant treatment would be an attractive therapeutic option, uptake is insufficient. The sodium iodide symporter (NIS) is responsible for thyroidal and mammary iodide uptake and deficient uptake of iodide is related to defects in the functional expression of NIS.