To test this hypothesis, we used results from the GABRIEL study, a consortium-based meta-analysis of asthma GWAS using 10 365 cases and 16 110 controls of European descent (31). We used the same integration approach described for the lymphocyte count GWAS. We were able to reject the null hypothesis that the asthma GWAS P-values for cis eQTL SNPs paired with the 117 lymphocyte count-associated genes were drawn from a null distribution (by permutation, P = 0.02; Fig. 5). Consistently, we found an enrichment of GABRIEL GWAS P-values smaller than 0.05 in the set of 117 genes (9.4%) compared with the corresponding well-calibrated genome-wide proportion of such P-values (5.3%; hypergeometric P = 0.044; Supplementary data, Table S6). These observations suggest that a subset of these 117 genes may be mediating asthma pathogenesis through changes in gene regulation, which affect lymphocyte activation.
