With regard to AML, we previously provided preliminary evidence that miR-181 may target elements of the “inflammasome” that ultimately lead to NF-κB activation and leukemia growth, while Li et al. showed that miR-181 promoted apoptosis, reduced viability and delayed leukemogenesis in MLL-rearranged AML by downregulating the homeobox gene PBX3 [28]. The gene discussed is KMT2A; the disease is acute myeloid leukemia.