The 10-year incidence rate of thrombosis in patients possessing the JAK2 mutation is 21%.[6] Hobbs et al reported that JAK2/V617F mutations might cause endothelial dysfunction to systematic arteries and veins, and promote leukocyte migration and PLT activation, ultimately leading to the formation of emboli that obstruct distal arteries.[7] Moreover, the heightened HCT in PV patients plays a significant role in blood viscosity, which might increase the hemocyte contact to vessel walls, resulting in the formation of localized thrombus and a subsequent increase in the incidence of stroke.[8]. The gene discussed is JAK2; the disease is acquired polycythemia vera.