Across nine models, expression of U5 snRNP200 was most prominent on AML cells from mice bearing the humanized inversion chromosome 3q21q26 allele (‘inversion 3 mice’)36,37 as well as simultaneous overexpression of fusion gene MLL-AF9 (also known as KMT2A-MLLT3) and NRASG12D cDNA (known as ‘RN2’ cells38). This evidence concerns the gene KMT2A and acute myeloid leukemia.