Graves’ disease (GD) is an autoimmune disorder characterized by hyperthyroidism and the presence of autoantibodies against the thyroid-stimulating hormone receptor (TSHR), which are classified as stimulatory, blocking, or neutral and which bind to different receptor epitopes. Binding of TSH to the TSHR, a member of the GPCR superfamily, leads to the activation of G proteins and, in response to receptor phosphorylation, the activation of ?-arrestin–dependent signaling.