The etiology and pathogenesis of hyperthyroidism have not yet been fully elucidated. However, TSH is often low or even undetectable in this disease as determined by radioimmunoassay, and it does not respond to TRH excitation test, and it can still develop after pituitary gland removal. The fact that the pituitary gland and thyroid axis are functioning normally in this disease, but TSH secretion is not increased, causes wood disease is not due to TSH. According to the research in the past 20 to 30 years, it has been proved that the development of the disease is mainly due to the autoimmune response induced by stress factors such as mental stimulation on a genetic basis. As early as 1956, Adams and Purves discovered a substance in the serum of patients with the disease that, when injected into guinea pigs, stimulated iodine uptake, synthesis and release of hormones, and hypertrophy of the gland, with effects similar to those of TsH, but slower and longer-lasting, so it was called long-acting thyroid stimulating substance (LATS). Since then, a large body of research has proven that this disease is an autoimmune disease, and indirect evidence includes: 1) a large number of lymphocytes and packed cells infiltrate the enlarged thyroid gland and the tissue behind the eye; 2) an increase in the absolute value and % of lymphocytes in the peripheral blood circulation, with hyperplasia of lymph nodes, thymus and visceral lymphoid tissue; 3) other autoimmune diseases of the thyroid gland occurring simultaneously or sequentially in the patient and his family, such as Hashimizu thyroiditis, mucinous edema, infiltrative thyroid disease, and mucosal edema. The rate of positive anti-thyroid and gastric antibodies in the blood of the patient and his family members is often high, as well as their full pricing. The direct evidence that the disease is an autoimmune disease includes: 1. In terms of humoral immunity, it is known that among the various antibodies against thyroid cell components, thyroid-stimulating antibodies, or thyroid-stimulating immunoglobulin (TSI) or TSH receptor antibodies (TRAb), which are used as antigens against TSH receptors, can be detected in 95% of the patients’ sera and have the ability to inhibit TSH and bind to TSH receptors or have the ability to close the TSH receptors. Tissue binding, which activates adenosine cyclase and enhances thyroid cell function. This antibody can cause neonatal hyperthyroidism through the placenta. In addition to the aforementioned sexual evidence, it has been confirmed that this antibody system is produced by B lymphocytes. There is no doubt that this disease is an autoimmune disease, but its pathogenesis is still speculative, especially because the cause of the initiation is unknown. It is believed that the genetic defect in the immune guardianship and regulation of the Ts cells of the patient may lead to the destabilization of the immune system and the loss of control of the “forbidden” cells during stress such as mental stimulation and infection, which results in the proliferation of TSI-producing B cells and the secretion of a large number of autoantibodies to TSI with the assistance of Th cells. The result is the proliferation of TSI-producing B cells, which secrete large amounts of autoantibodies to TSI with the help of Th cells and cause disease.