Accurately locating causal genes (‘fine-mapping’) for complex disorders is a challenge to GWAS and usually requires multiple approaches105. To highlight credibly causal variants, we used FINEMAP v1.139 at each of the 145 identified loci (Supplementary Table 3), selecting variants with a cumulative posterior probability of 95%. These were then annotated with ANNOVAR40 release 2016Feb1 (Supplementary Table 11). We mapped the SNPs with a FINEMAP posterior probability higher than 0.5 to the developing brain Hi-C data generated by Won et al.41, following the methodology described therein, which allowed us to implicate genes by chromatin interactions instead of solely chromosomal position (Supplementary Table 12). We compiled results from the eQTL analysis of the CommonMind Consortium post-mortem brain tissues44. This included 15,782 genes, which were curated to remove any genes with FPKM = 0 across >10% of individuals. All the SNPs from the meta-analysis data were mapped to the eQTL data using rs numbers, position and allele matching. Both datasets were analyzed together using SMR43, which resulted in 4,276 genes showing eQTLs with overlapping SNPs and genome-wide significant P values (Supplementary Table 13).
