These include: inhibiting the recruitment of CCR2+CD14++CD16– monocytes (TAM precursors), via CCL2-CCR2 blockade; specific deletion/depletion via anti-CD115/M-CSFR antibodies; and phenotypic/functional reprogramming to M1-like anti-leukaemia Mφs, through DICER inhibition-mediated upregulation of IFN-γ/STAT1-inducible genes and modulation of microRNAs. This evidence concerns the gene CCR2 and leukemia.