MLL has been shown to recruit NUP98 fusion proteins to its target genes and is required for the gene expression signature and proliferation of NUP98-r AML cells.14 The interaction between the N-terminal moiety of MLL and its cofactor Menin is critical in MLL-r leukemia, and therapeutic disruption of this association represents a promising targeting strategy that is under current clinical evaluation for this AML type. This evidence concerns the gene KMT2A and acute myeloid leukemia.