Acute myeloid leukemia (AML) is a stubborn malignant tumor, and AML with different mutations often exhibits significant heterogeneity, which poses challenges to the treatment of AML. RUNX1 is a vital transcription component participated in regulation of blood tissue development, and mutated RUNX1 are common in AML and are one of the typical mutations. Clinical studies have demonstrated that AML patients with mutated RUNX1 often have poor prognosis and lower survival rates, and have a worsening trend of bone marrow hyperplasia. Based on such patients, there is an urgent need for a more efficient treatment strategy that targets RUNX1 or its related factors to alleviate the adverse effects of RUNX1 mutations on AML patients. This article systematically examines RUNX1's function in the pathophysiology and prognosis of AML. From the perspective of the mechanism and patients, the impact of RUNX1 on AML and the relevant targeted treatment strategies currently being promoted are summarized and discussed. This article is dedicated to summarize the development direction and trends of current RUNX1 related AML treatment strategies, and deepen people's understanding of RUNX1-mutated AML.
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