While the aetiology of Graves disease is now well-established, treatment for Graves disease has largely remained unchanged for 50 years. However, relapse rates following antithyroid drug treatment remain high, destructive therapy to the thyroid is not without its short and longer-term risks and there have been limited studies of the benefits of different treatments in terms of long-term outcomes such as cardiovascular disease. There therefore remains much room for optimisation of our therapeutic approach. The advent of second generation assays for TSH receptor antibodies offers the possibility of targeted timing of the duration of antithyroid drug therapy and recent studies have improved predictive scores and identified additional factors such as serum selenium levels and common genetic variation that may modify the response to treatment. Prior thionamide therapy and the use steroids also modulate the response to radioioidine therapy. The duration of exposure to high thyroid hormone levels may impact on long-term cardiovascular and osteoporotic outcomes and new data is gradually becoming available that may influence the selection of therapy for Graves disease. B-cell therapy has recently been trialled for Graves disease and Graves orbitopathy and may improve remissions rates after anti thyroid drug therapy. New developments in blocking anti-TSH receptor monoclonal antibodies and the design of small molecule inhibitors of the TSH receptor may allow for more rapid induction of remission and improved outcomes especially in refractory disease.