The deletion of Mfn2 in the anorectic pro-opiomelanocortin (POMC) neurons of the hypothalamus disrupts endoplasmic reticulum (ER)–mitochondria contacts, ER stress activation, leptin resistance, and obesity (Schneeberger et al., 2013). Here, POMC is linked to obesity due to melanocortin 4 receptor deficiency.