Several pathophysiological mechanisms in obesity, e.g., oxidative stress, alterations in adipokine secretion, decreased adiponectin levels, increased inflammatory mediators, and increased activation of the renin–angiotensin system, may contribute to impaired microvascular dilatation and insulin-mediated capillary recruitment, leading to suboptimal glucose and insulin delivery to the skeletal muscle, and subsequent impaired glucose homeostasis [16,17,18,19,20]. The gene discussed is INS; the disease is Obesity.