A recurrent fusion of NUP98 with HOXA9 via chromosome translocation t(7;11)(p15;p15) drives AML by deregulating expression of MEIS1, HOXA9, and PBX3, arresting differentiation and inducing long-term proliferation of human HSCs (Takeda et al., 2006; Rio-Machin et al., 2017). This evidence concerns the gene MEIS1 and acute myeloid leukemia.