Endothelial nitric oxide synthase (eNOS)-generated NO relaxes vascular smooth muscle cells, increases blood flow, and represses the release of mediators that recruit proinflammatory cell populations to the endothelium [70,71]; NO produced by inducible nitric oxide synthase (iNOS) in adipocytes and proinflammatory macrophages is toxic levels and increased in obesity [72]; ROS are often substantially raised in obesity and gives rise to perilous pathological changes [73]. The gene discussed is NOS3; the disease is obesity due to melanocortin 4 receptor deficiency.