Furthermore, we analyzed whether treatment of MPN-derived BM-MSCs with the JAK1/2 inhibitor ruxolitinib, SMAD3 inhibitor SIS3 and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) inhibitor JSH23 or their combination could diminish the fibrotic phenotype. This evidence concerns the gene SMAD3 and myeloproliferative disorder.