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This review summarizes the role of SEs in maintaining hematopoietic lineage identity and examines how their dysregulation in acute myeloid leukemia (AML), myelodysplastic neoplasms (MDS), adult T-cell leukemia (ATL), acute lymphoblastic leukemia (ALL), and multiple myeloma (MM) leads to oncogenic activation. By regulating key oncogenes, SEs represent promising therapeutic targets. 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