Mechanistically, Barbier et al. showed in murine experiments using adoptive transfer of HSCs that had been retrovirally transduced with the human MLL-AF9 fusion oncogene that AML blasts exhibit an increased E-selectin-binding potential that enabled retention of AML blasts within the bone marrow and could contribute to chemotherapy resistance [21]. The gene discussed is KMT2A; the disease is acute myeloid leukemia.