Based on their NES, we selected biological processes and pathways that were significantly enriched in the low-EPAS1 expression phenotype, including ribosome, SRP-dependent cotranslational protein targeting to membrane, AML with MLL fusions, AML with FLT3-ITD, tretinoin response and PML-RARA fusion, and HDACS deacetylate histones. This evidence concerns the gene KMT2A and acute myeloid leukemia.