Intriguingly, JAK2-V617F expression had no major effect on platelet function; however, a series of elegant experiments, including bone marrow transplantation assays, showed that JAK2-V617F-positive endothelial cells (ECs) contribute greatly to dysfunctional hemostasis by inducing an acquired von-Willebrand syndrome (AVWS) phenotype [112]. This evidence concerns the gene JAK2 and acquired von willebrand syndrome.