Acute myeloid leukemia (AML) is a malignant disease of myeloid stem/progenitor cells, marked by the proliferation of immature myeloid cells in the bone marrow and blood, leading to anemia, bleeding, infection, fever, and organ infiltration.1 It accounts for 30% of pediatric leukemia, impacting molecular biology and chemotherapy, and most cases have a poor prognosis.2 While the exact etiology is unknown, it is related to regional factors, radiation, chemicals, alcoholism, smoking, and viral infections.3 Genetic mutations and biomarkers suggest a combination of genetics and environment.4 m6A is a common mRNA modification, but little is known about its role in AML. This study examines the genetic traits and prognosis of m6A regulators in AML, using TCGA-AML samples to explore the relationship between changes in m6A regulators and clinicopathology, thereby advancing our understanding of RNA epigenetics in AML.