Last, we found that stronger loops were formed between ECAD9 and CREs harboring TEAD3, STAT1, or SMAD family motifs (SI Appendix, Fig. S11E), consistent with the roles of these factors in regulating CDKN2A/B, which are diminished by the CAD risk variants (22, 23, 26). The gene discussed is CDKN2A; the disease is coronary artery disorder.