Because TP53 aberrations and complex karyotypes are known adverse risk features for AML [24, 25] and 21q22 amplification is not always seen in de novo AML, additional studies of larger cohorts are necessary to further determine whether 21q22 amplification is a new AML adverse biomarker for worse outcomes or just a secondary or passenger change as a result of co-existence of a complex karyotype, chromosome 7 abnormalities, or TP53 aberrations. The gene discussed is TP53; the disease is acute myeloid leukemia.