Specifically, core binding factor (CBF) AML with the presence of t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22) cytogenetic abnormalities, resulting in RUNX1/RUNX1T1 and CBFβ/MYH11 fusions, respectively, account for approximately 30% of pediatric AML [2]. This evidence concerns the gene CBFB and acute myeloid leukemia.