RECENT progress in the study of Graves' ophthalmopathy has been anything but stagnant. The past 20 yr have witnessed a rapid expansion in the collective understanding of basic pathophysiology, interdependence with thyroid pathology, and the effects of ocular or thyroidspecific therapy on disease course that threatens to erode the enigmatic nature of Graves' ophthalmopathy. In the past 5 yr alone, the central autoimmune target responsible for the hyperthyroidism of Graves' disease, the TSH receptor, has been cloned and sequenced (1,2), and an elucidation of exact antigenic epitopes using various techniques has begun (3–6). The availability of highly sensitive TSH assays has vastly simplified the diagnosis of subclinical hyperthyroidism (7), and improvements in TSH receptor autoantibody assays (8) have enhanced the ability of the clinician to identify subtle presentations of autoimmune thyroid disease. Exciting new work has suggested a primary pathogenetic role for the retroorbital fibroblast in the development and progression of Graves' ophthalmopathy (9, 10).