TF and metabolic syndrome: To prevent abnormal activation of coagulation, TF is not normally expressed in cells exposed to blood, such as endothelial cells or monocytes, but is highly expressed in subendothelial cells, including vascular smooth muscle cells (VSMCs) [16,25]; however, under pathological conditions, such as inflammatory diseases and dyslipidemia, activator protein 1 and nuclear factor-κB (NF-κB) increase TF gene expression in monocytes and endothelial cells, and this activates the extrinsic pathway, resulting in a thrombotic tendency [16,26,27].