In leptin-deficient ob/ob mice, loss of either Promch or MCH-containing neurons improved obesity, diabetes, and hepatic steatosis, suggesting that MCH is an important mediator of the response to leptin deficiency (Segal-Lieberman et al., 2003; Alon and Friedman, 2006). The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.