A treatment of AML cells with the specific CXCR4-SDF inhibitor, AMD3100 or antibodies against CD44, VCAM1, significantly sensitizes AML stem cells to treatment with chemotherapeutics, thus abrogating MSCs mediated chemoresistance and persistence of the minimal residual disease (Matsunaga et al., 2003; Tabe et al., 2007; Nervi et al., 2009; Jacamo et al., 2014). The gene discussed is CXCR4; the disease is acute myeloid leukemia.