In the present study, we hypothesized that VAT-derived FA are responsible for Kir2.1 dysfunction based on the following lines of evidence: i) VAT lipolysis is a major contributor to circulating levels of FAs in obesity [12–14]; ii) CD36 is a well-established FA translocase that appears to be required for Kir2.1 impairment under obesogenic conditions [19,23]; and iii) Kir2.1 has been shown to be inhibited by internal FA derivatives [25,26]. This evidence concerns the gene KCNJ2 and obesity due to melanocortin 4 receptor deficiency.