A continual challenge for gene expression profiling is that comparing expression levels of individual genes between alcoholic cases and controls may not be sufficiently powered to detect significant differences or determine causal candidate genes. Therefore, many researchers couple GWAS with expression quantitative loci (eQTL). An individual locus can account for a fraction of the genetic variance of a gene expression phenotype (Nica and Dermitzakis, 2013). Standard eQTL analysis involves a direct association test between markers of genetic variation and gene expression levels typically measured in hundreds of individuals (Nica and Dermitzakis, 2013). Genetic markers that are simultaneously associated with disease states are a powerful tool. For example, if one allele is more frequent in alcoholic cases than controls and is causal for gene expression effects of a nearby gene, that is known to be important for AUD, then it is probable that causality can be established (Nica and Dermitzakis, 2013). Among the enriched eQTL sets in the nucleus accumbens of human alcoholics, the most significant GWAS signals included the lncRNA PKI55 (Mamdani et al., 2015). This suggests a causal relationship
