Moreover, similar to what we had observed in HMGN1-OE ex vivo immortalized progenitors and HSPCs in vivo, HMGN1-OE plus AML-ETO9a leukemias had increased H3K27 acetylation, particularly within the subset of leukemia cells that had an HSC-like phenotype (Fig. 5g). The gene discussed is HMGN1; the disease is acute myeloid leukemia.