However, extensive preclinical studies including our own work have convincingly demonstrated that the level of radionuclide accumulation (radioiodide or alternative radionuclides such as 188Re and 211At) achieved in the tumor, the duration of radionuclide retention, and the distribution of NIS transgene expression was sufficient to reach a tumor dose within the range considered sufficient for a therapeutic response in thyroid cancer [56, 57]. The gene discussed is SLC5A5; the disease is thyroid gland carcinoma.