In recent years, significant advances have been made in defining genomic variations in normal karyotype AML patients, with the mutation status of nucleophosmin (NPM1), Fms-like tyrosine kinase 3 (FLT3), CCAAT/enhancer-binding protein alpha (CEBPA), isocitrate dehydrogenase 1/2 (IDH1/2), TET methylcytosine dioxygenase 2 (TET2) genes, etc. shown to be relevant [2,3]. This evidence concerns the gene NPM1 and acute myeloid leukemia.