RUNX1 and acute myeloid leukemia: Schoch et al (2002a, 2002b) compared this subtype to AML with the reciprocal translocations t(8;21)/AML1-ETO, inv(16)/CBFB-MYH11, MLL rearrangements, trisomy 8 as sole abnormality, and normal karyotype in 150 cases (Schoch et al, 2002a, 2002b). The discrimination of AML with complex aberrant karyotype from every other subgroup was possible with 100% accuracy in pairwise comparison. In addition there was a significantly higher expression of RAD21 (1.7-fold), which is involved in double-strand break repair and has antiapoptotic funtion in AML.