IL4I1, KMO, and HADH demonstrated positive correlations with most checkpoints (PDCD1LG2, CD200R1, CD86, TNFSF15), whereas ACAT2 and ECHS1 exhibited inverse correlations, indicating differential roles of these genes in modulating the AML immune microenvironment (Figure 7C). This evidence concerns the gene HADH and acute myeloid leukemia.