Our catalogue of fetal brain mQTLs provides a unique resource for investigating putative functional consequences of genetic variation associated with postulated neurodevelopmental disorders such as schizophrenia. A recent large-scale GWAS identified 108 independent genomic loci exhibiting genome-wide significant association with the disorder (P < 5×10−8), with evidence for a substantial polygenic component within signals that fall below this stringent level of significance12. Because the majority of these variants reside in regions of strong LD and do not index coding variants affecting protein structure, there remains considerable uncertainty about the causal genes involved in pathogenesis and the way in which they are functionally regulated by schizophrenia risk variants. We used PLINK31 to ‘clump’ our list of significant (P < 3.69×10−13) fetal brain mQTL variants into a set of quasi-independent SNPs (SNP pairwise r2 < 0.25 within 250kb (non-major histocompatibility complex (MHC)) or 10000kb (MHC)), see Online Methods) and tested for enrichment of schizophrenia-associated variants across a range of GWAS significance-thresholds, using up to 1,000,000 simulated SNP sets to generate empirical P values (see Online Methods). We observed a highly-significant enrichment (relative
