Because muscle is a significant glucose consumer when insulin levels are high, and because leanness improves sensitivity to insulin, it is not surprising that constitutive myostatin deficiency reduces hyperglycemia after a glucose challenge in mice with obesity-inducing mutations [6] and in mice fed a high-fat diet [1], [3], [4]. The gene discussed is MSTN; the disease is obesity due to melanocortin 4 receptor deficiency.