To ascertain the coordinated effects of trait-associated variants on gene expression, we used GWAS summary statistics to calculate PGSs for 1,263 traits in 28,158 samples (Methods, Supplementary Table 13). We reasoned that when the PGS for a trait correlates with the expression of a gene, the trans-eQTL effects of the individual risk variants (Figure 6a) converge on that gene, and it can be prioritized as a putative driver of the disease (Figure 6b).
