Using this criteria the unmethylated WT1 CpG island and hypermethylated AWT1 signature was extremely prevalent in AML patients, including individuals with the recurrent genetic abnormalities inv(16)(p13.1q22), t(16;16)(p13.1;q22) CBFB-MYH11, t(8;21)(q21;p22) AML1-ETO, t(15;17)(q22;q12) PML-RARA, t(9;11)(p22;q23) MLLT3-MLL, t(11; 10), inv(3), inv(9), NPM1 mutated and unspecified AML (Figure 4A, B). This evidence concerns the gene KMT2A and acute myeloid leukemia.