Gene expression and genotype data from lung, blood and multi-tissue resources were queried to identify whether the top variant at each of the 97 signals, or a proxy, were significantly associated with changes in expression of any gene (i.e. were an eQTL for any gene). Using this approach, and identification of deleterious variants within the association signal (Online methods, Supplementary Table 14), we implicated 234 genes with potentially causal effects on lung function (Supplementary Table 15). These 234 genes were enriched (False Discovery Rate (FDR) ≤5%) in elastic fibre pathways and in “signalling events mediated by the Hedgehog family”, the latter including CDON implicated by a novel intergenic signal (rs567508, between CDON and RPUSD4) on chromosome 11. We narrowed this group of 234 genes to 68 high-priority genes which were implicated via a deleterious variant or on stricter criteria for gene expression co-localisation (sentinel variant and top expression variant r2≥0.9, Table 2). We found that the 68 high-priority genes were overrepresented (FDR≤5%) among a number of gene ontology terms including SH3 domain binding, GTPase binding, actin binding and fibroblast migration
