In contrast, we did not find evidence for case-control differential expression among the implicated GWAS risk genes. At first blush this appears to contradict evidence for impact on risk. Yet the magnitude of differential expression will be determined largely by case-control differences in allele frequencies, which we know are small. Modeling the differential in allele frequencies and the predicted effect of alleles on gene expression demonstrates that the distribution of expected differential expression, across genes, is quite similar to the observed distribution from the CMC data (Fig. 7A). Using allele frequencies from the PGC schizophrenia data, we can ask what the number of cases are needed to detect differential expression. For example, 11,784 cases and 11,784 controls would be needed to have 80% power to detect a significant case-control difference in FURIN expression. Genome-wide, the median number of cases and controls needed to obtain 80% power assuming 10,000 genes is ~28,500, well beyond any available dataset (Fig. 7B,C). Our model demonstrates that the distribution of expected differential expression, across genes, is quite similar to the observed distribution from the CMC
