Furthermore, given that Evi1 heterozygosity ameliorates CML-CP and CML-BC development and that the combination of Evi1 and BCR–ABL causes acute myeloid leukemia resembling CML-BC, Evi1 could regulate CML development as a potent driver. This evidence concerns the gene RUNX1 and chronic myelogenous leukemia, BCR-ABL1 positive.