results suggested that GWAS risk and eQTL association signals co-localized for 84 genes in 30 of these loci (adjusted P < 0.05; Supplementary Fig. 6A, Supplementary data file 2). After removing genes where additional evaluation indicated lack of consistency (Supplementary Fig. 7B), there were 33 genes highlighted in 18 of the 108 GWAS loci (Supplementary data file 2). Genes found to have variants affecting risk for autism are often found enriched for variation affecting risk for SCZ; indeed, compared to other genes with eQTL in the GWAS loci, these 33 genes are more enriched for nonsynonymous de novo mutations in autism (fold enrichment = 2.4, Pcorrected = 0.03), although not for SCZ, intellectual disability, or epilepsy.
