in the inclusion of weakly associated SNPs with both gene expression and lymphocyte count. On the one hand, this approach was more resistant to possible sampling biases (e.g. due to spurious signals from gene- or SNP-dense regions of the genome). On the other hand, we acknowledge that this property of our study also limits the ability to explain any individual association by a regulatory change affecting a nearby gene. That said, the evidence for association with lymphocyte count was significantly stronger for the subset of genes found using our approach compared with the null expectation when we considered genes expressed in LCLs but not included in our test set. This observation provides overall support for a connection between the most significant GWAS loci and variation in gene regulation.
