In addition to these mechanisms governing suppressed NK cell function leading to poor NK cell-mediated targeting of leukemic cells, data from a pre-clinical animal model on de novo AML along with collected NK cell from patients with AML have indicated that the microRNA (miRNA) miR-29b, a regulator of T-bet and Eomes, can be elevated in NK cells via AML cell-induced activation of the transcription factor aryl hydrocarbon receptor that directly up-regulates miR-29b expression resulting in incomplete maturation and poor cytotoxicity (96, 139). The gene discussed is EOMES; the disease is acute myeloid leukemia.