Although platelets are involved in different processes such as triggering inflammation, fighting microbial infection, promoting tumor metastasis, and embryonic blood/lymphatic vessel separation their principal function still remains stopping hemorrhage following vascular injury. Upon tissue trauma platelets initially tether and roll over the exposed extracellular matrix, a process that eventually results in firm platelet adhesion and that triggers a signaling cascade mediated by tyrosine kinases and G-protein coupled receptors, resulting in full platelet activation with concomitant granule release. Released effectors in turn recruit and activate additional platelets, next leading to platelet aggregation and the presentation of a pro coagulant surface promoting formation of a fibrin-rich haemostatic plug. Platelet activation, in addition, also triggers endothelial cells to locally synthesize and secrete molecules that limit thrombus formation.