In leukemia, our prior research found that GNE‐987, a von Hippel‐Lindau‐based Proteolysis Targeting Chimera (PROTAC) targeting the critical SE reader Bromodomain containing 4 (BRD4), can inhibit the expression of a range of SE‐driven genes and hinder the survival of T‐ALL and acute myeloid leukemia (AML) cells.[20, 21, 22] In this study, to identify new key oncogenes in T‐ALL, we built profiles of SEs by analyzing ChIP‐seq data from clinical samples and cell lines. This evidence concerns the gene BRD4 and leukemia.