By leveraging the power of a large-scale GWAS approach, we identified common genetic etiology for GERD in COPD, which supports the epidemiological link between GERD and COPD and begins to provide a mechanistic foundation for the therapeutic utility of the STAT3, GPCR, and oxidative stress signaling pathways as modulators in both GERD and COPD. The gene discussed is STAT3; the disease is gastroesophageal reflux disease.