The ITGB5 association did not replicate in two independent populations, nor was there any evidence that the corresponding SNP was an eQTL of ITGB5. The AGFG1 result replicated at a nominally significant level in one independent population of COPD subjects (LHS P-value 0.012), and the SNP had a nominally significant unadjusted P-value (0.0067) for being eQTL of AGFG1. While future functional studies are required to validate the potential involvement of these SNPs in modulating AHR, current knowledge of both genes suggests that our associations may represent biologically significant findings. Here, AHR is linked to chronic obstructive pulmonary disease.