Since the CMC cases bear an aggregate common polygenic schizophrenia risk burden, we subsequently performed an independent controls-only analysis (using limma) of the effect of polygenic risk scores on expression of each gene. While no single gene was found to be significantly associated with PRS after correction for multiple testing using an FDR approach (cutoff of 5%), there was inflation of the P value distribution101 consistent with a non-uniform distribution (π1 = 0.22). Moreover, there was a significantly positive, but small, correlation (Pearson r = 0.095, p < 10−16) between the independent t-statistics for the effect of PRS on expression in controls and those we found for case-control expression differences in the full cohort, consistent with at least some of the SCZ case-control differences in CMC perhaps being driven by underlying genetic differences between the SCZ cases and controls.
