Several studies have demonstrated that SE-associated genes are particularly downregulated in cancer cells treated with CDK7 inhibitors.340 For example, neuroblastomas driven by MYCN amplification, which induces aberrant SEs, are disproportionately vulnerable to CDK7 inhibition.346 Similarly, the oncogenic transcription factor RUNX1 in T cell acute lymphoblastic leukemia (T-ALL) is driven by SE and repressed by CDK7 inhibition. Here, CDK7 is linked to T-cell acute lymphoblastic leukemia.