Specific MFN2 knockout in these neurons decreased α-MSH release, altered mitochondrial morphology, decreased mitochondrial-ER contacts and ER stress, reduced the conversion of POMC into α-MSH, developed leptin resistance due to ER stress, increased ROS production due to impaired complex I activity, increased energy intake, decreased energy consumption, and finally lead to obesity [150]. The gene discussed is POMC; the disease is obesity disorder.