We found that, compared with wild type (WT), Asxl1+/−, or Nf1+/−, compound haploinsufficiency of Asxl1 (Asxl1+/−) and Nf1 (Nf1+/−) in mice (Asxl1+/−;Nf1+/−) resulted in the increased frequency of long-term HSCs (LT-HSCs) in the marrow, increased genome-wide H3K4me3 occupancy, which accelerated myeloid malignancies, and development of pronounced anemia and thrombocytopenia (i.e., MDS, MDS/MPN, and myeloid leukemia) [64]. The gene discussed is NF1; the disease is myeloid neoplasm.