CXCL12 and myelodysplastic syndrome: While this provides a rationale for the cell-intrinsic modulation of SDF-1 transcription in response to TGFß ligands, it remains to be seen whether the GDF-11-mediated functional inhibition of MSCs in MDS in vivo is a cell-intrinsic mechanism or is extrinsically mediated by other cells within the BMME [33].