Thrombosis in MPN patients is a multifactorial event involving chronic inflammation [65], functionally hyper-reactive PLTs produced by direct megakaryocyte differentiation pathway from platelet-biased HSCs [66] and other complex interactions among various blood cells [16], so role of these processes and cell types in the thrombosis risk caused by the Jak2-R1063H mutation cannot be excluded. Here, JAK2 is linked to myeloproliferative disorder.