Although the studies utilised the MLL-AF9 genetic murine model of AML, discrepancies between findings could be due to the authors focusing on potentially phenotypically different Mφ subsets i.e., Keech et al. (2017) centring on CD11b–F4/80+CD169+VCAM1+ and Yang et al. (2017) focusing their attention on CD3–GR1lowMCSFRintF4/80hiSSClow Mφs (Table 1). This evidence concerns the gene KMT2A and acute myeloid leukemia.