The most common chromosomal translocation in AML (10% of total AML) is t(8;21), which generates the AML1-ETO oncofusion protein and is mostly associated with a favorable prognosis [1, 2] The t(8;21) translocation is considered to be the initiating (driver) hit for further AML development and can sometimes already be observed in utero [3]. The gene discussed is RUNX1; the disease is acute myeloid leukemia.