Thus, it is possible that IL-1β released by residual AML blasts may alter the BM microenvironment and suppress the proliferation of NK cell precursors [85] Finally, AML blasts may induce the expression of the transcription factor aryl hydrocarbon receptor (AHR) that activates miR-29b in NK cell precursors impairing their maturation and functions [86]. This evidence concerns the gene IL1B and acute myeloid leukemia.