Zfp521 has also been implicated in the induction of B-cell lymphomagenesis [27] and is significantly overexpressed in many acute myeloid leukemias (AMLs), particularly in those transformed by the oncogenic fusion protein MLL-AF9, coherently in MLL-rearranged AML cell lines and primary ex vivo MLL-AF9 expressing cells, ZNF521 depletion blocks AML progression [28,29,30,31,32]. This evidence concerns the gene KMT2A and acute myeloid leukemia.