Gang of 3 in aggressive CLL?

tion in response to platelet agonists, and to platelet morphological changes resembling the human disease. Although MYH9-related human disorders such as May-Hegglin anomaly are autosomal-dominant in inheritance,4 and therefore myosin-IIA deficiency is less extensive,4 altered contractile activity during primary hemostasis may contribute to the bleeding episodes that affect some patients. The current work by Ono and colleagues in Shaun Jackson’s group implies that myosin-IIA complexes play a key role not only in the birth of the platelet, but also in the endgame of hemostatic plug formation and thrombus consolidation in the vessel wall. Because the thrombus is attached to the vessel wall, the contraction will pull the thrombus toward the lesion, simultaneously cementing the breach and facilitating blood flow through the vessel. In the context of atherothrombotic disease, the extent of the contraction may affect the resistance of platelet-rich clots to fibrinolytic agents and to antiplatelet drugs. Conflict-of-interest disclosure: The author declares no competing financial interests. ■