Possible explanations are dyslipidemia, hypertension, and diabetes, or chronic inflammation-mediated oxidative stress, insulin resistance, subclinical inflammation via increased secretion of IL-6, C-reactive protein and plasminogen activator inhibitor-1, endothelial dysfunction, cytokine upregulation, atherogenic dyslipidemia, postprandial lipemia, pro-coagulation, and hypofibrinolysis [33,34,35,36,37,38,39]. This evidence concerns the gene CRP and hypertensive disorder.