Variants associated with CAD are located within intronic and 3′ flanking sequences and recent data suggest that these, and other variants in close proximity, mediate risk of CAD by altering expression of ANRIL (and possibly decreasing expression of CDKN2A and CDKN2B) via multiple, independent cis-regulatory elements [34], [35] and, more specifically, by influencing the expression and structure of individual splice variants produced from the ANRIL gene [36], [37], [38], [39], [40]. Here, CDKN2A is linked to coronary artery disorder.