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 enrichment = 4.11, P = 3.0×10−6) of genome-wide significant schizophrenia risk variants amongst fetal brain mQTLs, with a trend for stronger enrichment at more stringent levels of GWAS significance (Supplementary Fig. 9 and Table 1). To examine the specificity of any enrichment, these analyses were repeated using large GWAS datasets from i) a non-neurodevelopmental brain disorder (Alzheimer’s disease (AD)32) and ii) two non-neurological phenotypes (body mass index (BMI)33 and type 2 diabetes (T2D)34. Although our confidence in the enrichment of fetal brain mQTL in these datasets is limited by the smaller number of semi-independent GWAS SNPs, levels of enrichment were found to be notably lower for all other tested phenotypes (Table 1). Variants associated with AD are, however, nominally significantly enriched at the most relaxed GWAS threshold (GWAS threshold P < 5×10−5: relative enrichment = 3.18, P = 0.022) and several individual GWAS variants identified for this and the other tested phenotypes are also significant mQTLs in fetal brain mQTLs
