Given the statistical enrichment between locations of early developmentally regulated CpGs and genetic risk for SZ, we attempted to directly determine the association between risk genotype among the genome-wide significant loci of SZ and DNAm levels. We genotyped and imputed these samples to the 1000 Genomes reference panel, and retained 7,426,085 common SNPs (MAF > 5%, see Methods) for methylation quantitative trait loci (meQTL) analysis to understand how common genetic variation influences DNAm levels. Here we reintroduced probes on the sex chromosomes (as genotypes across the genome should not correlate with sex) as well as probes with annotated SNPs at the target CpG site (as these could represent true biological signal), while still removing probes with annotated SNPs at the single base extension site (which represent technical signal if associated with genotype), leaving 477,636 CpGs for analysis. We conducted a meQTL analysis in the adult control samples (age > 13, N=258) allowing for up to 20kb between SNPs and CpGs, controlling for factors related to ancestry and global epigenetic variation (see Methods), and identified 4,107,214 significant SNP-CpG methylation associations (meQTLs)
