This communication between hypoxia-inflammation-oxidative stress leads to proinflammatory cytokine and adipokine production, such as leptin, TNF-α, and IL-6 and the negative regulation of anti-inflammatory mediators, such as adiponectin and IL-10, thus aggravating endothelial dysfunction, resulting in the loss or attenuation of the anti-contractile action of PVAT in obesity (Xia and Li, 2017). The gene discussed is LEP; the disease is endothelial dysfunction.