BACKGROUND Monoclonal antibodies have become a mainstay in the treatment of autoimmune, viral and malignant disease. Many adverse reactions to antibody therapy are unpredictable and include endocrinopathies. The monoclonal antibody alemtuzumab is licensed for the treatment of MS but induces Graves’ disease in 22% of patients receiving the drug for this indication. Alemtuzumab targets CD52 which depletes mature lymphocytes. In this case report, a patient who developed Graves’ disease following alemtuzumab therapy is discussed and clinical considerations and pathophysiology are reviewed. CASE DESCRIPTION SK is a 37-year-old woman diagnosed with MS at 25, and also suffers from depression. SK began alemtuzumab treatment at aged 35, subsequently, she was found to have deranged TFTs (TSH <0.01 mU/L and fT4 28 pmol/L). SK experienced regular palpitations, fatigue and disturbed sleep. The patient attributed her fatigue and palpitations to MS and did not seek medical attention. SK reported no other symptoms of hyperthyroidism. Symptoms resolved following administration of carbimazole and propranolol. DISCUSSION The exact mechanisms underlying both MS and alemtuzumab-induced Graves’ disease are unknown. Lymphocyte depletion and reconstitution are thought to cause autoimmunity by the over-repopulation of naïve B-cells, modulation of T-lymphocytes and disruption of cytokine signalling (IL-21 and IFNy). The slow regeneration of Treg cells that normally promote tolerance underlies these changes. This report identifies several clinical challenges, including the detection of adverse reactions to new medications, ensuring thorough symptom reporting, and the fragility of quality of life in patients with MS.