They also showed that the clonogenic capacity of HSCs significantly improves by knocking down CD33 in the cocultured MDSCs, and vice versa, CD33 could repress myelopoiesis when it was overexpressed in healthy donor-derived MDSCs, suggesting that the downstream activated pathways may play a role in the BM failure of the MDS patients. The gene discussed is CD33; the disease is myelodysplastic syndrome.