Autoimmune thyroid disease is characterized by the presence of autoantibodies against various thyroid components, namely the thyrotropin receptor, thyroid peroxidase, and thyroglobulin, as well as by inflammatory cellular infiltrate of variable severity within the gland. Among the autoantibodies found in autoimmune thyroid disease, thyrotropin receptor autoantibodies (TRAb) are most closely associated with disease pathogenesis. All forms of autoimmune thyrotoxicosis (Graves disease; GD, Hashitoxicosis, neonatal thyrotoxicosis) are caused by the production of stimulating TRAb-. These autoantibodies, also known as long-acting thyroid-stimulator (LATS) or thyroid-stimulating immunoglobulins (TSI), bind to the receptor and transactivate it, leading to stimulation of the thyroid gland independent of the normal feedback-regulated thyrotropin (TSH) stimulation.