In addition, JAK2 mutation is involved in activating the leukocyte and the coagulation cascade, in endothelial injury, in producing of leukocyte–platelet aggregates.[3] The presence of leukocyte–platelet aggregates and microparticles (endothelial cell platelet aggregates) in blood circulation is more common in patients with ET and PV. This evidence concerns the gene JAK2 and essential thrombocythemia.