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. The gene discussed is FLT1; the disease is acute myeloid leukemia.