Medical researchers report on a new mechanism that controls blood cell function and several possible molecular targets for treating myelodysplasia syndromes (MDS) — a group of pre-malignant disorders in which bone marrow does not produce enough healthy blood cells. MDS can lead to acute myeloid leukemia (AML), a fast-spreading blood cancer that can be deadly if not treated promptly. The authors report that overexpression of a protein called TRAF6 in hematopoietic (blood) cells drives the onset of MDS.