Others cannot, including failure of JAK2 V617F to enhance MPN HSC bone marrow pool size (14), resistance of MPN HSC to tyrosine kinase inhibitors (15) premature release of mutated CD34+ HSC from the bone marrow (16), myelofibrosis or the clinical presentation of PV and PMF as isolated thrombocytosis, suggesting that pathways other than constitutive JAK2 activation are involved. This evidence concerns the gene CD34 and myeloproliferative disorder.