Although, the number of SNP-array lesions appeared very low in CBF-AML, when combining with sequence analyses, we were able to identify recurrent involvement of known and potentially new cancer genes including FOXP1 loss-of-function in inv(16)-AML, ZBTB7A homozygous mutations through CN-LOH in t(8;21)-AML and CCDC26 disruption in both genetic subgroups of CBF-AML. This evidence concerns the gene CEBPZ and acute myeloid leukemia.