Significant advances in understanding the genetic architecture of schizophrenia (MIM: 181500) have occurred within the last 10 years. However, for common variants identified in genome-wide association studies (GWASs), the success in locus identification is not yet matched by an understanding of their underlying basic mechanism or effect on pathophysiology. Expression quantitative trait loci (eQTL), which are responsible for a significant proportion of variation in gene expression, could serve as a link between the numerous non-coding genetic associations that have been identified in GWASs and susceptibility to common diseases directly through their association with gene expression regulation.1, 2, 3, 4 Accordingly, results from eQTL mapping studies have been successfully utilized to identify genes and causal variants from GWASs for various complex phenotypes, including asthma (MIM: 600807), body mass index (MIM: 601665), celiac disease (MIM: 212750), and Crohn disease (MIM: 266600).5, 6, 7, 8