According to the traditional theory, the pathogenesis of VTE is associated with abnormalities in blood flow, vessel integrity and blood components. Therefore, we compared gene expressions of these VTE related factors in patients with PE and without PE. Among the expressions of coagulation factor genes, only gene expressions of factor Ⅶ and FIBCD1 were significantly elevated in patients with PE compared with patients without PE. As for genes of other coagulant factors, the expression value of patients with PE was either not significantly different or less than those patients without PE in comparison. There was no significant difference between two groups of patients in gene expression of anticoagulant proteins. And so was in gene expression of fibrinolytic factors except plasminogen Urokinase receptor (PLAUR, Fig.1 ). L-selectin, ITGAL and ICAM-1 are the adhesion molecules originated from different family, mainly distributed on the surface of lymphocytes. ICAM-1 is the ligand of ITGAL which is member of integrin family. Significantly elevated mRNA expression of these adhesion molecules in PE group indicate activated adhesion function of white blood cells. However, mRNA expression of P-selectin (mainly distributed on the surface of ECs and platelets) and E-selection (mainly distributed on the surface of activated ECs) are not elevated in PE group which indicate venous endothelial cells are not impaired in patients with PE (Fig.2) . In expression of platelet aggregation related genes, only 2 genes (GP6 and PAFAH1B2) were significantly elevated in the patients with PE. Compared to patients without PE, the expressions of 3 in 7 genes of platelet adhesion function were significantly increased in patients with PE. As for genes of platelet releasing, the expression of one gene was significantly up and down regulated between 2 groups of patients, respectively (Fig.3 ).