TGFB1 and myelofibrosis: PTPRC and TGFβ were chosen because we have previously reported a reduction in PTPRC expression18 and upregulation of TGFβ expression15 induced by a range of other leukaemogenic oncogenes.19 In addition, TGFβ plays an important role in the pathogenesis of CML20 and myelofibrosis.21 Western blot analysis of PTPRC expression in the presence of activated JAK2 mutants (Figure 1a) demonstrated decreased levels compared with control cells.