Fig. 6
Genes regulated by disease-associated eQTL SNPs differ across diseases. Within each disease, permutation-based p values for gene-level disease association were calculated by combining the strongest significant cis-eQTL SNPs in each cell type. As in Table 1, proxy eQTL SNPs in each genetic dataset were filtered for relative independence before computation of a permutation-based disease association p value. P values were corrected within each disease by the Benjamini–Hochberg FDR method. The heatmap represents the negative logarithm of these corrected values such that genes marked in white-to-red shades show disease association, FDR < 0.1. Grey indicates no data available because the GWAS dataset did not include SNPs that tagged eQTLs for this gene with LD r2 ≥ 0.8. Gene colours on the left side correspond to TNFSF ligands (yellow), TNFRSF receptors (orange) and adaptors/signalling molecules (black) as in Fig. 2. Genes are presented in order of decreasing association with any disease