Hnisz et al. [5] introduced two deletions found in T-ALL patients using CRISPR/Cas9 at anchors of insulator loops containing the oncogenes TAL1 and LMO2. The authors showed that the deletions increased interactions between enhancers and promoters that were insulated by anchor elements in the wild type cells leading to upregulation of TAL1 and LMO2 in the edited cells. The gene discussed is LMO2; the disease is acute lymphoblastic leukemia.