Clinical outcomes are particularly poor for AML subtypes with contain chromosomal abnormalities, such as t(8;21) translocation, which accounts for 40% to 80% of M2 type AML (AML-M2) [1].AML1-ETO fusion proteinis generated by t(8∶21) translocation [2], which is thought to be a transcriptional repressor of AML1 target genes. The gene discussed is RUNX1T1; the disease is acute myeloid leukemia.