Using our polished data sets derived from distinct case and control subjects (see Methods and Supporting Information S1), we succeeded in identifying a cluster of genome-wide significant SNPs associated with POAG in CDKN2B-AS1, a non-coding gene with an unknown function, on chromosome 9p21.3 (Figure 2A, B) . Several variants in chromosome 9p21 have been found to be associated with a variety of common diseases, and 9p21 was initially identified as a locus for coronary artery disease (CAD) [20] [21] [22] [23] and type-2 diabetes [24] [25] [26] . However, little is known about the biological meanings underlying the locus, as 9p21 is a ''gene desert'' locus and most of the variants identified were noncoding. Recently, Harismendy et al. [27] reported that they have identified 33 enhancers in 9p21, some of which being within CDKN2B-AS1, and it turned out to be the second densest gene desert for predicted enhancers, thus suggesting the regulatory role of sequences residing within non-coding loci. They finally determined a few adjacent, as well as distant (.45 kb), target gene regions relevant to CAD biology physically interacting with the enhancer by 3D-DSL (also known as ''4C''), a chromatin conformation capture technology, in human vascular endothelial cells. Overall, their study has provided an excellent example of a solution to link the unknown meanings of statistical association to a biological function. Since the POAG variants were also identified in CDKN2B-AS1, the variants would probably affect the expression level of the downstream genes CDKN2A and CDKN2B. In fact, Burdon et al. reported up-regulated CDKN2A and CDKN2B expression in response to the elevated IOP [14] , suggesting the involvement of the locus in molecular pathways leading to glaucoma development. Moreover, the possibility that the variants would also affect the distant unidentified target genes in the context of the complex etiology of glaucoma, as well as the nature of the identified locus [27] , cannot be ruled out.