On the other hand, mice with a POMC-specific deletion of MFN2 (mitofusin 2), a key protein for mitochondrial fusion and the formation of ER–mitochondria contacts, display a loss of these interactions, defective POMC processing, ER stress-induced leptin resistance, and obesity (228). The gene discussed is MFN2; the disease is obesity due to melanocortin 4 receptor deficiency.