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. The gene discussed is UCN2; the disease is acute myeloid leukemia.