In acute myeloid leukemia (AML) harboring MLL rearrangement (MLL-r AML), the complex assembled by WDR5 and wild-type (WT) MLL cooperates with the MLL-r chimeric oncoproteins to sustain an oncogenic gene expression program, and depletion of the WDR5-MLL1 complex suppresses the growth of MLL-r AMLs (5–7). The gene discussed is KMT2A; the disease is acute myeloid leukemia.