Graves’ disease (GD) is an autoimmune disease that affects multiple systems including the thyroid, orbits and skin.1 Graves’ orbitopathy (GO) is the most common (in 25-50% of GD patients) and serious clinical manifestation of extrathyroidal GD.2 It has been shown that hyperthyroidism in GD results from the stimulation of thyroid stimulating hormone (TSH) receptors located on thyrocytes by immunoglobulin G, which is continuously produced by B cells. This evidence concerns the gene TSHR and geroderma osteodysplastica.