NK cell homing to and retention within the BM has been shown to correlate with improved acute myeloid leukemia (AML) control (15, 32) However, the chemokine TME is sufficiently skewed during MM development, whereby CXCL12 downmodulation is paralleled by increased expression of CXCR3 cognate ligands, creating pathological conditions generally restrictive to NK cell infiltration (22). This evidence concerns the gene CXCL12 and acute myeloid leukemia.