For example, in AML, chromosomal rearrangements reposition SEs to drive EVI1 or MYC overexpression (Roe et al., 2015; Gröschel et al., 2014; Ottema et al., 2021), while in T-ALL, SE-mediated TAL1 activation sustains leukemogenesis (Smith et al., 2023). This evidence concerns the gene TAL1 and acute myeloid leukemia.