A 30-year-old Caucasian lady was diagnosed with type 2 diabetes in July 2005 on an oral glucose tolerance test and was treated with metformin. Sixteen months later she presented with urinary symptoms and was noted to have 2+ ketonuria. Her blood glucose was 13.4 mmol/l. Her BMI was 26 kg/m2 and she was noted to have Cushingoid habitus and acanthosis nigricans. Her blood pressure was normal. Her serum sodium was 130 mmol/l, potassium 3.7 mmol/l and bicarbonate 8 mmol/l. She was noted to have severe hypertriglyceridaemia of 58.4 mmol/l. Serum cholesterol was 16.1 mmol/l. She was treated with intravenous insulin and discharged home on twice daily pre-mix insulin. Investigations for Cushings syndrome were negative. 24 h urinary free cortisol was normal. 0900 h serum cortisol after overnight dexamethasone suppression test was 36 nmol/l. ACTH was 6 ng/l. Cyclical Cushings was considered but six 24 h urinary free cortisol collections were negative. Despite taking ~300 units of insulin her HbA1c remained above 11% on a basal bolus regimen. Anti GADA was negative. Genetic analysis confirmed severe hyperinsulinaemia with dyslipidaemia with very low adiponectin and high leptin levels, in keeping with patients with Cushingoid body habitus. On the basis that she could have a PPARγ gene mutation she was commenced on pioglitazone with marked improvement of her diabetes control and sharp reduction in insulin requirement. HbA1c improved from 11.8 to 7.5% in 3 months. Subsequently the sequence of her PPARγ gene has been reported to be normal. Her diabetes control has subsequently deteriorated with her most recent HbA1c being around 12%. Should we still investigate further for cyclical Cushings syndrome?