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Graves΄ disease (GD) was one of the first human autoimmune diseases to be characterized following the discovery of thyroid-stimulating antibodies in hyperthyroid patients in 1956 (1  ). GD is now known to be the most common cause of hyperthyroidism between the ages of 20 and 50 years. In females, the annual incidence ranges from 15 to 200 per 100,000 per year (2  ). The rates observed in males are about one tenth of those in females, and the disease is more common in iodine-sufficient regions (3  ). The hyperactivity of the thyroid gland is due to the presence of thyroid stimulating antibodies, and these are now known to recognize and activate the thyroid-stimulating hormone receptor (TSHR). These TSHR stimulating antibodies increase the growth and the function of the thyroid follicular cells, leading to the excessive production of thyroid hormones (both T3 and T4) and symptoms of tachycardia, anxiety, and weight loss among others. Pathologically, the disease is characterized by a heterogeneous lymphocytic infiltration of the thyroid parenchyma as well as infiltration of retroorbital and dermal tissues (4–6  ) (see Chap. 31). Transplacental antibody transferred to the infants of affected mothers during pregnancy can induce symptoms similar to the mother by causing neonatal Graves΄ disease (7, 8  ). Similarly, antibodies from patients with GD when injected into experimental animals and even humans can induce thyroid activation (9  ). [ABSTRACT FROM AUTHOR]