Given that most of reported cases have been associated with B-lineage ALL and are associated with JAK2 positivity [9, 10], and that JAK2 mutation has been detected in B/NK/T-lymphoid precursors from PV and PMF patients [11, 12], it has been speculated that the aberrant JAK2 tyrosine kinase activity in a common myelo-lymphoid CD34 + progenitor may play a causative role and contribute to lymphoid transformation. This evidence concerns the gene JAK2 and acquired polycythemia vera.