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]. This evidence concerns the gene NPM1 and acute myeloid leukemia.