Valk et al (2004) used unsupervised cluster analyses and identified up to 16 groups of AML based on separate molecular signatures. The clustering was driven not only by the presence of chromosomal lesions (e.g., t(8;21)/AML1-ETO, t(15;17)/PML-RARA, inv(16)/CBFB-MYH11), but also by particular genetic mutations (CEBPA, MLL-PTD, FLT3-LM) and abnormal oncogene expression (EVI1). This evidence concerns the gene KMT2A and acute myeloid leukemia.