Larger number of alterations were located in chr 1, 2, 11, 13, and 19 and distributed along genes that have previously showed to be involved in the pathogenesis of AML, such as KMT2A, FLT3, ETV6, RUNX1 and HNPRK. Losses and CN-LOH were concentrated in chr 1, 2, 5q, 7, 11q and 13q. This evidence concerns the gene RUNX1 and acute myeloid leukemia.