The possible explanations might be: 1) ANRIL upregulated transcription of CAD-related protein coding genes including p15INK4b and p16INK4a to increase proliferation and migration in arterial smooth muscle cells and vascular smooth muscle cells, thereby contributing to high risk of CAD and increased stenosis degree of coronary artery; 2) ANRIL induced endothelial dysfunction via accelerating several signaling pathways such as TNF-α-NF-kB-ANRIL and YY1-IL6/8 pathways, thereby inducing inflammatory responses in pathological processes of CAD. This evidence concerns the gene CDKN2A and endothelial dysfunction.