Given the ubiquitous importance of gene expression variance to phenotype, the known heritability of gene expression variance, and the great preponderance of non-coding functional elements in the genome [50], complex disease studies can benefit from eQTL analyses. Towards that end, we searched for correlations between replicated eQTL SNPs identified here and complex trait associated SNPs (R2>80%; Table 2, Table S4) in the NHGRI GWAS catalog (http://www.genome.gov/gwastudies/). These included several previously characterized mechanistic links to complex traits, such as VKORC1 expression and warfarin drug response [51] and SORT1 expression correlations with lipid levels and heart disease [13], both of which were originally identified using the UW liver panel described here. Additionally, these data support a relationship, which had previously been speculated but not shown to exist, between NOD2 expression levels and leprosy risk [48], and novel hypotheses such as a link between expression of the uncharacterized C2orf43 gene and prostate cancer risk [52].
