In visceral obesity, excess VAT is characterized by the hormone leptin hypersecretion and infiltration of activated macrophages, leading to the release of inflammatory cytokines (e.g., interleukin 6, tumour necrosis factor-α), which induce insulin resistance, endothelial dysfunction, hypercoagulability, and systemic inflammation, thereby facilitating the atherosclerotic process [5,52]. The gene discussed is LEP; the disease is endothelial dysfunction.