Interestingly, in contrast to the mild phenotype observed following the early developmental deletion of Lepr from Agrp neurons, ablating Lepr from Agrp neurons in adults promotes dramatic hyperphagia and obesity (9–11), consistent with developmental compensation for early perturbations to Agrp neurons (12) and suggesting that the hyperphagic obesity of Lepr-null mice must result from the loss of Lepr in non-Agrp neurons (such as LepRbGlp1r cells). The gene discussed is AGRP; the disease is obesity due to melanocortin 4 receptor deficiency.