A current view of vascular thrombosis emphasizes the importance of cellular surface biochemistry and the integrated contribution of platelets, monocytes and endothelial cells that contribute to atherothrombosis. Initiation of coagulation occurs on tissue-factor bearing cells, while amplification (or priming) requires activation of platelets and coagulation proteases. The final phase, propagation is determined by thrombin generation on platelet surfaces [1] (Fig. 1). The cell-based model of vascular thrombosis highlights specific phases or biochemical stages rather than a more traditional view of independent coagulation pathways or cascades. Accordingly, tissue factor is considered the key element for initiation of thrombosis, wherein its ability to complex with factor (f) VIIa and activate f X ultimately causes thrombin generation. Although thrombin is a pivotal enzyme in coagulation and thrombosis, the importance of fXa and its diverse effects on thrombin generation, inflammatory processes, smooth muscle cell proliferation and endothelial cell activation warrants serious consideration as a potential target for pharmacologic intervention.