In cytogenetically normal AML patients, miR-181 contributed to a better clinical outcome by regulating Toll-like receptors and interleukin-1β, while in cytogenetically abnormal AML, miR-181 contributed to a better clinical outcome by regulating HOXA7, HOXA9, HOXA11 and PBX3 [115]. The gene discussed is HOXA9; the disease is acute myeloid leukemia.