Potentially a differential degree of induced vascular damage may underlie these differences, with an increased contribution of thrombin, TF and TF-induced hypercoagulation to the increased prothrombotic response observed by Ortillon et al,20 whereas collagen and platelet GPVI increasingly contribute to FeCl3-induced thrombus formation upon more severe vascular damage,21 which may be presented by the hyperlipidemic ApoE knockout mice used in our study to mimic the increased proinflammatory, dyslipidemic condition of many CKD patients.22 This evidence concerns the gene GP6 and chronic kidney disease.