Conclusions
We have identified a novel locus on 11p15.5, which includes several biologically plausible candidates (EFCAB4A, CHID1 and AP2A2) as potential CB susceptibility genes. We have also found significantly increased effect sizes of FAM13A SNPs in COPD subjects with CB compared to those without CB. Although our secondary GWAS of CB versus no CB within COPD subjects did not show genome-wide significant SNPs, a locus including ATF6 should be explored for its related functional consequences. This study supports the concept that different genetic susceptibility contributes to phenotypic heterogeneity within COPD.