By potently inhibiting Mc4r signaling, this combination is implicated in the hyperphagia, obesity, and diabetes of leptin-deficient models, and reversal of this effect is implicated in the restoration of euglycemia to diabetic animals following central administration of either leptin (33) or FGF1 (5). The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.