A 47-year-old female presented to the Emergency department following an episode of loss of consciousness at home that her daughter had identified as due to hypoglycaemia (using her husbands capillary blood glucose meter 1.1mmol/l) and treated. She reported several episodes of fainting, sweating and generalised weakness over 6 months which improved after eating snacks. There was no previous history of diabetes; she had been diagnosed with Graves disease 6 months previously, following unintentional weight loss of 7 kg over 4 months, treated with carbimazole. Her past medical history included hypertension, arthritis, functional neurological disorder and migraine. She lived with her family from which it was noted her husband and sister were on oral medications for diabetes. On clinical examination, her BMI was 24 kg/m2. Pigmentation was noted on the dorsal aspect of her neck but overt acanthosis nigricans or features of insulin resistance were not found. Hourly CBG monitoring was carried out during her inpatient stay. She continued to experience recurrent spontaneous episodes of hypoglycaemia (four episodes over 24 hours). The differentials considered included insulin autoimmune syndrome (Carbimazole-associated insulin autoimmune syndrome), use of diabetes medications, insulinoma or tumour related hypoglycaemia. The investigations revealed: glucose 2.5mmol/l, insulin 1539 pmol/l(18-173 pmol/l), c-peptide 5605 pmol/l(370-1470 pmol/l), TSH: 0.01mIU/l, free T4 18.7 pmol/l, free T3 4.3 pmol/l, TSH-receptor antibody 3.42 IU/l, HbA1c 37mmol/mol, cortisol 510nmol/l. Adrenal antibodies, coeliac screen and pituitary profile were found to be within reference range. Sulphonylurea screen and Insulin antibodies were also requested. No focal abnormality was identified on MRI pancreas. Carbimazole was stopped and she was discharged with a flash glucose monitor. She was followed up in the outpatient clinic when she reported eating every 2-3 hours to avoid hypoglycaemia. It was found that insulin antibodies were elevated in keeping with insulin autoimmune syndrome (Hirata disease); additionally, a plasma sulphonylurea screen was also positive, a source for which was not identified by the patient. On repeat testing after 9 months: sulphonylurea screen was negative, laboratory blood glucose 4.8mmol/l, insulin 60 pmol/l, c-peptide 830 pmol/l. Insulin autoimmune syndrome was considered to be in remission. Radioactive iodine was considered as the treatment of choice should she require treatment of Graves disease.