In addition to mutations found in genes including NPM1, CEBPA, DNMT3A, TET2, RUNX1, ASXL1, IDH2, and MLL, dysfunctional receptor tyrosine kinases (RTKs) such as Flt, VEGFR or c‐Kit have been shown to be drivers of the progress of AML.5, 8 Therefore, it would be valuable to discover whether effective existing kinase inhibitors restrict AML tumors. This evidence concerns the gene RUNX1 and acute myeloid leukemia.