Whereas their study specifically investigated sequence-driven loss of Ctcf binding at proximal, intra-TAD enhancer regions, we observed that H3K9ac-depleted promoters in Kat2a KO leukemia cells had a significant association with experimental Ctcf binding in ENCODE experiments, and we speculate that Ctcf may be dislodged to enhancers and promote asymmetric distribution of histone acetylation marks, with dysregulation of locus control. This evidence concerns the gene CTCF and leukemia.