Abstract: Acute myeloid leukemia (AML) is a disease with marked heterogeneity in both response to therapy and survival. Numerous genetic mutations which cannot be identified by cytogenetic detection have been found including gene mutations in Fms-liketyrosine kinase 3 (FLT3), nucleophosmin 1 (NPM1), and CCAAT enhancer-binding protein-α (CEBPA). Furthermore, the panel of known molecular markers is continuously increasing,for example,considering the recently described isocitrate dehydrogenase (IDH1/2) and Wilms Tumour 1 gene (WT1) mutations. This review focuses on the structures and features of these gene mutations,as well as their influence on the prognosis of AML.