This might result from: 1) ANRIL participated in the transcription process of protein coding genes on 9p21.3 locus (such p15 INK4b and p16INK4a ) to increase cardiovascular cells proliferation and migration, thereby advancing CAD conditions and leading to unfavorable OS in CAD patients; 2) ANRIL aggravated inflammatory responses through stimulating several pathways including TNF-α-NF-kB-ANRIL and Yin Yang 1 (YY1)-IL6/8 pathways, leading to progressive inflammatory responses and poor OS in CAD patients. The gene discussed is CDKN2B-AS1; the disease is coronary artery disorder.