This work supports the hypothesis that they can be classified into several categories: abnormalities common to all AML (e.g. 8q24.3 gain or 17q11.2 deletion involving NF1); those more frequently found in t-AML (e.g. 7q21 or 7q33 deletions or even the specific gain of HOX genes); and those specifically found in p-AML (e.g. loss of the 139 to 152.8 Mb of 7q, 11q24 gain or 21q22 with amplifications of ERG and ETS2). The gene discussed is ETS2; the disease is acute myeloid leukemia.