It has been postulated that the mutant JAK2 causes increased proliferation of granulocytes and platelets which in turn, leads to bone marrow fibrosis by producing large quantities of stimulatory cytokines, such as transforming growth factor-beta (TGF-β), platelet-derived growth factor (PDGF), and fibroblast growth factor-beta (FGF-β).[3,7,9] The exact role of JAK2V617F in bone marrow fibrosis remains to be determined. Here, TGFB1 is linked to primary myelofibrosis.