DNA methylation (DNAm), an epigenetic modification to cytosine, is involved in mediating the developmental regulation of gene expression and function, as well as transcriptional processes such as genomic imprinting and X chromosome inactivation.1, 2 Although often regarded as a mechanism of transcriptional repression, the relationship between DNAm and gene expression is highly complex and not fully understood.3 Gene-body DNAm, for example, is often associated with active expression4 and also influences other transcriptional processes, including alternative splicing and promoter usage.5 This dynamic property of DNAm means it can vary across samples and might underlie phenotypic differences. There is growing interest in characterizing the variation of DNAm across populations6, 7 and in the role of DNAm in disease, and recent epigenome-wide association studies (EWASs) have identified robust associations between variable DNAm and cancer,8 as well as a diverse range of other complex phenotypes, including rheumatoid arthritis [MIM: 180300],9 body-mass index,10 schizophrenia [MIM: 181500],11 and Alzheimer disease [MIM: 104300].12 Characterizing the complex relationship between genetic, epigenetic, and transcriptomic variation will increase understanding about the mechanisms underpinning health and disease phenotypes. Twin and family studies have demonstrated that population-level variation in DNAm is under considerable genetic control, although these effects vary across genomic loci, developmental stages, and different cell and tissue types.13, 14, 15, 16, 17 Studies in a variety of tissues, including brain, whole blood, pancreatic islet cells, and adipose tissue, have identified widespread associations between common DNA sequence variants and DNAm.17, 18, 19, 20, 21, 22 These DNAm quantitative trait loci (mQTLs) are primarily cis-acting, are enriched in regulatory chromatin domains and transcription-factor binding sites, and have been shown to colocalize with gene expression quantitative trait loci (eQTLs).3, 17, 23