Tumor necrosis factor-(TNF-), a proinflammatory cytokine, plays a prominent role in obesity-associated insulin resistance and-cell dysfunction (1) and, therefore, in the development of diabetes. An association between obesity and elevated TNF-levels and, furthermore, the substantial decline of TNF-levels with the simultaneous restoration of insulin sensitivity during weight loss was reported by Dandona et al.(2). Recently, we found evidence that prolonged administration of anti–TNF-antibody is able to improve insulin sensitivity in insulin-resistant subjects (3); this finding has been confirmed by Kiortsis et al.(4). Here, we report a case demonstrating the relapse of diabetes in a former type 2 diabetic patient after an interruption of prolonged treatment for psoriatic arthritis with infliximab, an anti–TNF-antibody. The improvement in insulin sensitivity of this patient has been reported along with post hoc evidence that chronic administration of infliximab improves insulin resistance in a small sample of patients with inflammatory joint diseases (3). The patient, a 33-year-old male with a BMI of 22.4 kg/m2, had been treated with infliximab continuously until April 2003. From April 2003 to October 2003, infliximab was stopped due to remission of psoriatic arthritis. Readministration of infliximab was started again in October 2003 because of increased disease activity. In the interval without infliximab treatment, we observed a significant increase of fasting capillary blood glucose (monitored by self measurement) from a mean of 4.93 0.18 mmol/l in the preinterruption period to 6.77 0.26 mmol/l in the infliximab-free period (Fig.