RUNX1/ETO (RE), the t(8;21)-derived fusion protein, is present in 12% of de novo acute myeloid leukemia (AML) cases and up to 40% of M2 subtype AMLs according to the French–American–British classification.1 Recently, a truncated form of RE (REtr), which lacks the C-terminal N-CoR/SMRT-interacting domain, has been identified, recapitulating a naturally occurring highly leukemogenic splice variant RE9a observed in AML patients.2, 3 RE harbors the DNA-binding domain of RUNX1 fused to the nearly entire nuclear co-repressor ETO protein. This evidence concerns the gene NCOR2 and acute myeloid leukemia.