While the mouse model of AML used in our studies mimics 11q23-translocations involving the MLL gene rearrangement and fusion, the human AML cell line KG1a exhibits a complex karyotype with several structural aberrations, including FGFR1OP2-FGFR1 gene fusion, NRASG12D mutation and TP53c.672+1G→A splice donor mutation, but no translocation involving either MLL or AML1 genes (Mrózek et al., 2003). The gene discussed is RUNX1; the disease is acute myeloid leukemia.