Although the mechanism underlying myelofibrosis associated with JAK2 (a MPL W515L stimulated target) induced MPNs has been reported to be the excess production of TGFβ by CD34+ cells [48] the importance of TGFβ to the pathogenesis of myelofibrosis and its utility as a therapeutic target in treatment of JAK2 induced MPN are still not clear. This evidence concerns the gene TGFB1 and myelofibrosis.