Functional inhibition of MSCs in MDS, leading to defective osteogenic differentiation capacity, is also mediated by TGF-β, present at increased levels in the MDS BMME (50), which cause abnormal gene expression of PITX2, HOXB6 and TBX15, leading to phenotypic and functional deficits (76). Here, TGFB1 is linked to myelodysplastic syndrome.