Given the extended region of high linkage disequilibrium at the 9p21.3 locus and the large number of transcriptional regulatory elements that are present in the CAD risk region, it is currently not entirely clear whether the risk of CAD and PD is mediated solely by ANRIL or whether its neighbors, CDKN2B and CDKN2A - two well-known tumor suppressor genes involved in cell cycle arrest and malignant transformation in certain cancers (30) - contribute to the mechanism. The gene discussed is CDKN2B; the disease is coronary artery disorder.