Because activating mutations in receptor tyrosine kinases are present in at least 30% of patients with AML, multiple studies investigated their cooperation with RUNX1‐ETO by retrovirally transducing murine bone marrow cells with RUNX1‐ETO and either the TEL‐PDGFβR fusion protein, the c‐KIT N822K and D814V mutations, the Flt3 length mutation (FLT3‐LM) or NRasG12D mutation into lethally irradiated syngeneic mice.20, 21, 22, 23, 24, 25. The gene discussed is RUNX1; the disease is acute myeloid leukemia.