Transposon-accessible chromatin sequencing (ATAC-seq) has demonstrated that CCTC-binding factor (CTCF) sites, which are often sensitive to methylation status, are engaged in short-term HSC, repressing a host of quiescence pathways [18, 19, 21]; CTCF binding has also been shown to be aberrant in AML, with enrichment of CTCF binding at motifs for key myeloid transcription factors such as CEBPA, PU.1, and RUNX1 [20]. This evidence concerns the gene RUNX1 and acute myeloid leukemia.