Previous studies, mainly performed in myelofibrosis models, indicate that the mutant/malignant megakaryocytes contribute to the development of fibrosis by increased expression of fibrotic and pro-inflammatory cytokines and interleukins, growth factors (including transforming growth factor-β (TGF-β)), extracellular matrix components, and other factors [1]. Here, TGFB1 is linked to myelofibrosis.