Although the shorter latency of AE9a/Asxl2-null leukemias over AML1-ETO/Asxl2-null leukemias is likely to reflect the known enhanced leukemogenicity of AE9a over AML1-ETO (ref. 41), future efforts to decipher if there is a specific functional collaboration between AE9a and ASXL2 loss may be enlightening. The gene discussed is ASXL2; the disease is leukemia.