One way in which eQTL may affect gene expression is through alteration of cis-regulatory elements such as promoters and enhancers. Putative causal eSNPs have been shown to be enriched in genomic regions containing functional annotations such as DNase hypersensitive sites, transcription factor binding sites, promoters, and enhancers.51, 52, 53, 54 Our observation that conditional eQTL fall farther from transcription start sites than primary eQTL led us to hypothesize that primary eQTL may affect transcription levels by altering functional sites in promoters whereas conditional eQTL may do so by altering more distal regulatory elements such as enhancers. We therefore assessed enrichment of primary and conditional eQTL in brain active promoter (TssA) and enhancer (merged Enh and EnhG) states derived from the NIH Roadmap Epigenomics Project,32, 33 and in H3K4me3 and H3K27ac neuronal (NeuN+) and non-neuronal (NeuN−) ChIP-seq peaks from a subset of the CMC post-mortem DLPFC samples. The overlap of H3K4me3 and H3K27ac ChIP-seq peaks was used as a proxy for active promoters, and H3K27ac peaks that do not overlap H3K4me3 peaks were used as a (relatively non-specific) proxy for enhancers.33 We performed logistic regression of SNP status (eQTL versus random matched SNP) on overlap with functional annotations, separately for each eQTL order (primary, secondary, and greater than secondary).