In conclusion, the demethylase ALKBH5 downregulates ATOX1 by reducing its m6A levels, thereby modulating cuproptosis in AML-a mechanism that offers potential novel insights and therapeutic targets for AML treatment.<h4>Significance</h4>This study reveals that in AML, the demethylase ALKBH5 downregulates ATOX1 expression by reducing its m6A modification, thereby inhibiting cuproptosis and promoting AML progression. This evidence concerns the gene MBD2 and acute myeloid leukemia.