Our work provides strong statistical support for association with moderate-to-severe or severe COPD susceptibility for three previously-described9–17 (CHRNA3/5/IREB2, HHIP, and FAM13A) and three additional (RIN3, MMP3/MMP12, TGFB2) loci. We provide evidence that additional GWAS in larger samples are likely to identify additional genetic determinants of COPD, and suggest using subsets of COPD (such as severe disease) may provide additional insight to genetic risk factors. Our work also suggests further studies to elucidate biological mechanisms77, which we hope will reveal new insights into COPD pathogenesis, and ultimately, treatment for this important disease.
