There is increasing evidence that formation of a stable hemostatic plug requires adhesive and signaling events that continue beyond the onset of platelet aggregation. These events are facilitated and, in some cases, made possible, by the persistent close contacts between platelets that can only occur when platelets begin to aggregate. Participants include integrins and other cell adhesion molecules, secreted agonists, receptor tyrosine kinases, and protein fragments that are shed from the surface of activated platelets. Collectively, these molecules promote the continued growth and stability of the hemostatic plug.