Several co-expressed genes and enriched pathways point towards an AML inflammatory phenotype, characterized by expression of IL6, IL10RA, CXCL10, THEMIS2, TNFAIP3, LILRA5, LILRB2. ADM was also upregulated in the CD4+ and CD8+ T cell subsets from AML patients compared with healthy controls and ADM correlating genes that were identified in AML, participate in a signature of immune tolerance in CD4+ T cells. Here, TNFAIP3 is linked to acute myeloid leukemia.