In 2005, the discovery of the constitutively activating JAK2V617F mutation in the majority (97%) of patients with polycythemia vera (PV) and approximately 50% of patients with idiopathic myelofibrosis (MF) confirmed the central role played by JAK2 in the pathogenesis of myeloproliferative neoplasms [7–9]. This evidence concerns the gene JAK2 and acquired polycythemia vera.