We chose to investigate the impact of selectively restoring Pomc function in the developing hypothalamus from a conditionally silent allele (FneoΔ2 mice) using a Vglut2-IRES-Cre knock-in mouse model (Vong et al., 2011) and then determine how restoration of Pomc expression only in the glutamatergic subpopulation of POMC neurons shapes hypothalamic POMC neural circuitry and impacts energy balance in the obesity-destined mice. This evidence concerns the gene POMC and obesity due to melanocortin 4 receptor deficiency.