Acute myeloid leukemia (AML), as a heterogeneous disease caused by several specific mutant genes (such as FLT3, NPM1, DNMT3A, IDH1, IDH2, TET2, fusion genes, and so on), is characterized by increased proliferation of abnormal myeloid progenitors with blocking terminal differentiation in BM and other tissues [1]. The gene discussed is FLT3; the disease is acute myeloid leukemia.