For each of the schizophrenia associated loci, we identified a credible causal set of SNPs (for definition see Supplementary text). 36 In only 10 instances (Supplementary Table 4) was the association signal credibly attributable to a known nonsynonymous exonic polymorphism. The apparently limited role of protein coding variants is consistent both with exome sequencing findings 33 and with the hypothesis that most associated variants detected by GWAS exert their effects through altering gene expression rather than protein structure37,38 and with the observation that schizophrenia risk loci are enriched for expression quantitative trait loci (eQTL).39
