Consistent with the reciprocal effects of the BDNF-TrkB and glucocorticoid-GR pathways on the regulation of the HPA axis54 is that deletion of the BDNF receptor TrkB in cholecystokinin (CCK)-GABAergic neurons resulted in HPA-axis hyperactivity and obesity in mice66. The gene discussed is BDNF; the disease is obesity due to melanocortin 4 receptor deficiency.