The role of platelets in the formation of arterial thrombus on atherosclerotic plaque are well documented. However in early disease, platelets also appear to play a role in promoting the recruitment of inflammatory leukocytes. We have recently described a paradigm in which the recruitment of monocytes to TGF-β1 stimulated endothelial cells (EC) is mediated by platelet bridges. TGF-β1 promotes the expression of a matrix of Von Willebrand factor (VWF) on the EC surface which recruits platelets from flowing blood. Upon platelet activation at the EC surface by ADP, monocytes are in turn recruited by platelet P-selectin. The Src family kinases (SFKs) play an important role in platelet activation during haemostasis and we propose that these signalling molecules could represent targets for intervention in platelet mediated monocyte recruitment during atherogenesis. Dasatinib, a broad spectrum SFK inhibitor, ablated ADP dependent aggregation of both human and murine platelets and inhibited the activation of platelets and the secondary recruitment of monocytes on substrates of immobilised VWF or on TGF-β1 stimulated EC. In addition, platelets from the Lyn-/- but not the Fgr-/- mouse, showed deficiencies in aggregation in response to ADP. These data strongly imply that targeting specific SFK members could inhibit platelet dependent recruitment of monocytes in atherogenesis, and these may represent drugable targets for intervening in the chronic inflammatory processes that support atheroma formation.