A possible explanation for the discrepancy between the uptake at the level of the primary mass and metastases could be that the function of the sodium iodide symporter, which is responsible for radionuclide uptake, disappears at the level of the tumor during the course of the disease (loss of differentiation), whereas it could be preserved at the level of metastases, that may display a different pattern of expression of thyroid‐specific proteins.22, 31. The gene discussed is SLC5A5; the disease is neoplasm.