MDS patients carrying mutations in TET2 are more likely to respond to HMA treatment7, but mechanisms of action of HMA on MDS cells are still unclear and could involve the BM microenvironment, including immune (lymphocytes, myeloid-derived suppressive cells)8 and non-immune partners (mesenchymal stromal cells)9. The gene discussed is TET2; the disease is myelodysplastic syndrome.