Co-culture experiments showed that ALKBH5 knockdown enhanced the proportion of CD8<sup>+</sup> T cells and secretion of IFN-γ/TNF-α, and reduced the survival rate of AML cells.<h4>Conclusions</h4>ALKBH5 may promote AML progression and immune escape through the upregulation of PD-L1 and modulation of T-cell function, which provides a theoretical basis for the development and screening of novel immunotherapeutic strategies for AML. This evidence concerns the gene CD8A and acute myeloid leukemia.