A feature of MetS is increasing adipose tissue, which secretes various adipokines and cytokines, including leptin, adiponectin, interleukin, and nitric oxide; these factors cause megakaryocytes to produce larger platelets.[5,33] Additionally, vascular endothelial cells are severely damaged in patients with MetS, and endothelial dysfunction might also trigger the same mechanisms.[5,34] Insulin resistance is a crucial mechanism underlying MetS. The gene discussed is LEP; the disease is endothelial dysfunction.