Accordingly, in recent years, it has become clear that altering the function of DUB affects HSC homeostasis and may contribute to the onset of MDS and AML (Figure 4) by several mechanisms [254], as described for the DUBs BAP1, a tumor suppressor that cooperates with the polycomb group protein ASXL1 [255,256,257] or A20 [258,259], BRCC3 [260,261,262], USP7 [263,264], and USP10 [265]. The gene discussed is ASXL1; the disease is myelodysplastic syndrome.