Of the 108 SCZ GWAS loci previously reported3, 73 harbor cis-eQTL SNPs for one or more genes (FDR ≤ 5%). To determine if 73 out of 108 loci were larger than that expected by chance, we conducted an experiment that randomly chose such loci in the genome; it showed that 73 loci with cis-eQTL SNPs is consistent with chance expectation (data not shown). Moreover, the simple presence of an eQTL does not imply disease causality. We used Sherlock 25, a Bayesian approach that prioritizes consistency between disease association and eQTL signatures in GWAS loci, to identify genes likely to contribute to SCZ etiology. While Sherlock evaluated genes across the genome, we only evaluated genes within the 108 SCZ GWAS loci because SNPs in these loci showed genome-wide significant association with SCZ; thus, in essence, we fine mapped these loci. The 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
