Mutations, such as FLT3-ITD (Fms-like tyrosine kinase-3 internal tandem duplication), nucleophosmin 1 (NPM1), and RUNX1-RUNX1T1 (RUNX1 translocation partner 1), play pivotal roles in the pathogenesis and clinical outcomes of AML [5,6]. This evidence concerns the gene RUNX1T1 and acute myeloid leukemia.