Potential mechanisms for these findings in SCH patients include oxidative stress in mitochondria due to increased plasma inflammatory markers, insulin resistance, activation of thrombosis and hypercoagulability, endothelial dysfunction, delayed diastolic filling, impaired left ventricular systolic function, and increased vascular resistance [6,23,24,25,26,27,28,29]. The gene discussed is INS; the disease is endothelial dysfunction.