Graves’ disease (GD) is the commonest cause of hyperthyroidism, accounted for 70-80% in iodine sufficient countries and up to 50% in iodine deficient countries. Combination of genetic predisposition and environmental factors influences the development of GD. Graves’ orbitopathy (GO) represents the most common extra-thyroidal manifestation of GD with substantial impact on morbidity and quality of life. Expression of thyroid stimulating hormone receptor (TSHR) mRNA and protein in orbital tissues infiltrated by the activated lymphocytes produced by thyroid cells (Thyroid Receptor Antibody) results in the secretion of inflammatory cytokines that leads to the development of histological and clinical characteristics of GO. A subdivision of TRAb, thyroid stimulating antibody (TSAb), was found to have a close relationship with the activity and severity of GO, and suggested to be considered as a direct parameter of GO. Here, we present a 75-year-old female with a history of GD that has successfully been treated with radioiodine treatment, who developed GO 13 months after therapy while being hypothyroid with high TRAb level. The patient was given a second dose of radioiodine ablation to maintain GO with successful result.