A variety of JAK2 variants that activate tyrosine kinases have been reported, including the well-known V617F variant which occurs in most patients with polycythemia vera and approximately half of the patients with essential thrombocytosis and primary myelofibrosis.1–5 Many of these patients will respond favorably to JAK2 inhibitors.6,7 Translocations and rearrangements involving JAK2, however, are less common. This evidence concerns the gene JAK2 and acquired polycythemia vera.