Collectively, the physiological consequences from SELENOP-aAb that can be deduced from the data would predict intracellular Se deficiency, low GPx and DIO biosynthesis rate, impaired TH activation in SELENOP-target cells with local hypothyroidism, reduced iodide liberation causing low urinary iodine, and elevated oxidative stress in kidney and elsewhere (Fig. 5). The gene discussed is SELENOP; the disease is hypothyroidism.