Robust improvements in glucose homeostasis have been reported in response to 11β-HSD1 inhibitors in both murine models of diabetes and obesity and in phase II clinical trials in patients with type 2 diabetes and metabolic syndrome, with reductions in fasting insulin, blood glucose, HbA1c, and HOMA2-IR (7, 10, 13, 35, 39-41). The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.