Acute myeloid leukemia (AML) is a malignant clonal disease characterized by the impaired proliferation and differentiation of myeloid immature cells, leading to the dysfunction of normal hematopoietic function (1) .There is a lot of evidence showing that the occurrence and the development of AML are often accompanied by the emergence of gene fusions (e.g., PML::RARA, CBFB::MYH11, and RUNX1::RUNX1T1, among others) and mutations such as c-KIT, FLT3-ITD, NPM1, and TP53 (2, 3). Here, RUNX1 is linked to acute myeloid leukemia.