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Hemostasis is complex. The process of hemostasis has several outcomes, including physiologically arresting blood loss at sites of vascular injury. In simple terms, this is achieved by formation of a “plug that seals the hole.” This “plug” comprises a framework of blood components that act together to create a stable mass that stops further blood leakage. Hemostasis involves the complex interaction of many integrated processes.1 Central to hemostasis is the blood milieu, containing platelets, which in part act like “bricks,” and many adhesive plasma proteins, which in part act like “mortar,” working together to develop a framework that we sometimes call the “platelet plug.” However, neither the platelets nor the plasma proteins are passive agents in this process. When hemostasis works, everything is in physiological balance, and we are not even cognizant of this activity taking place in our own bodies. When hemostasis gets out of balance, however, disease or pathological processes can occur. Plasma is complex, but platelets are even more complicated.2,3 This journal has published several papers onplatelet physiology, and the ongoing popularity of these papers attests to the complexity of platelet physiology and their interest in our readership.4,5 Each individual platelet expresses a huge number of proteins on their surface that we call platelet receptors, and these interact with many plasma components including other proteins. There are around 100 million platelets in each mL of our blood. Hemostasis can be conveniently separated into primary and secondary hemostasis, with primary hemostasis reflecting predominantly vesselwall and platelet activity (including adhesion), and secondary hemostasis mainly reflecting the plasma coagulation system (including clot formation).1 Although this provides a convenient separation to help teach hemostasis to junior scientists, and to study this process in vitro, it needs to be recognized that, in vivo at least, these systems do not work in isolation. Primary and secondary hemostasis work in concert to form the platelet plug. Injury to a blood vessel causes a cascade of events. The injury releases cellular components including “tissue factor,” as well as exposing subendothelial surfaces that are normally not exposed to this blood. This causes activation of “secondary hemostasis” by several mechanisms. Sometimes we use terms such as the “coagulation cascade,” but the important elements here are generation of thrombin and conversion of soluble plasma protein fibrinogen to “insoluble” fibrin. The vessel injury also leads to platelet activation and platelet adhesion to the damaged site. Integral to the process of platelet adhesion are the platelet receptors andmany plasma proteins, including von Willebrand factor (VWF), which act as a kind of sticky string to “glue” the platelets together and fasten them to the damaged subendothelial surface.6 Platelets aggregate to form the scaffolding of the platelet plug, and the entire structure is further stabilized by the fibrin being formed, as robustly integrated into the platelet plug. Indeed, much hemostasis activity goes into creating the platelet plug. In normal physiology, this platelet plug seals the hole, and thus permits wound healing to subsequently occur. However, if the process of hemostasis is dysfunctional, pathological situations can ensue. On one side of this unbalanced hemostasis is where hemostasis may be “underactive” and patients can bleed (e.g., if the plasma components or platelets do not work as well as they should, the formation of the platelet plug may be delayed, or else it may not be formed properly). If hemostasis is “over-active,” patients may be at increased risk of thrombosis. In such situations, the platelet plug may grow too large and block off

Commentary: Controversies in Thrombosis and Hemostasis Part 2–Does Sticky Platelet Syndrome Exist?