We had previously shown that treatment with plerixafor renders infant MLL-R leukemic blasts more susceptible to the FLT3 inhibitor lestaurtinib in a xenograft model.[9] To increase the applicability of this treatment strategy in this difficult-to-treat population, we combined a standard chemotherapeutic agent with plerixafor in a xenograft model of infant MLL-R ALL. This evidence concerns the gene FLT3 and acute lymphoblastic leukemia.