Focusing on a murine model of MLL-AF9 driven AML, preliminary findings from Keech et al. (2017) demonstrate that specific depletion of CD169+/SIGLEC1+ Mφs (Table 1), using heterozygous diphtheria toxin (DT) receptor expressing mice to selectively deplete host CD169+ Mφs via DT injection, significantly enhanced the median survival of mice treated with cytarabine and doxorubicin, as compared to AML counterparts exhibiting normal levels of BM CD169+ Mφs. Here, KMT2A is linked to acute myeloid leukemia.