In acute myeloid leukemia (AML), a high level of STAT5 expression drives histone lactylation, upregulates the transcription of PD-L1, and induces CD8+ T cell exhaustion, indicating that modulating the PD-1/PD-L1 axis might counteract STAT5-induced immunosuppression (112). This evidence concerns the gene CD8A and acute myeloid leukemia.