Since glaucoma shows familial aggregation and its prevalence varies between individuals of different ethnicities, it has been theorized that genetic factors play a significant role in the pathogenesis of glaucoma [8, 9] . Therefore, several institutions are making profound efforts to discover single-nucleotide variants for glaucoma by conducting a genome-wide association study (GWAS) [10] [11] [12] [13] [14] , and there are a few published reports of the association of particular loci, such as the CAV1/CAV2 locus (7q31.1) [13] and the TMCO1 or CDKN2B-AS1 loci (1q24.1 or 9p21.3, respectively) [14] , with POAG using Caucasian subjects. However, it appears that a controversy still exists as to determining the authentic variants associating with POAG, even within the same ethnicity of European descent [14, 15] . We previously reported a GWAS and the subsequent follow-up study focused on the high-ranked variants identified in the initial population using in total of 1,575 Japanese subjects [10] . We identified six variants located in three loci, 1q43, 10p12.31, and 12q21.31, on the chromosome which were modestly associated with POAG, although the association results were not reproducible with a different population of different ethnicities [13, 16, 17] . In that previous study, we combined the patients from both HPG and NPG subtypes as a single case group in order to increase the statistical power [10] . Therefore, the genetic loci that were identified are most likely to be components of the molecular mechanism shared by both subtypes. Another Japanese group performed a GWAS [12] and discovered variants in SRBD1 on 2p21 and ELOVL5 on 6p12.1 that were associated with NPG (in that study, NPG was referred to as ''normal tension glaucoma'') [18] . However, since the findings in that study were derived from a single population, replication studies to support those findings still need to be conducted.