Examining roles for direct leptin action on neurons that contain specific neurotransmitters revealed that although ablating Lepr from glutamatergic neurons decreases energy expenditure and promotes mild obesity, ablating Lepr from GABAergic cells produces hyperphagic obesity approaching that of db/db mice (Vong et al. 2011). The gene discussed is LEPR; the disease is obesity due to melanocortin 4 receptor deficiency.