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). Here, STAT1 is linked to coronary artery disorder.