Table 1 presents the 11 genetic loci with common SNPs/indels implicated at genome-wide significance (P<5×10−8) and replicated in one or more independent datasets for the same phenotype/biomarker or extended to a related smoking phenotype/biomarker. The UGT2B10-UGT2A3 locus was identified in cotinine biomarker GWAS, but this finding has not been extended to smoking phenotypes [32]; the 10 other GWAS-identified loci influence susceptibility of smoking phenotypes. Lead SNPs with the smallest P value from each distinct genetic locus are presented, although several loci include many significantly associated SNPs, often strongly correlated with the lead SNPs. For example, 360 SNPs in the CHRNA5-CHRNA3-CHRNB4 locus were significantly associated in GWAS meta-analysis of FTND-defined nicotine dependence [21], and 719 SNPs in the CYP2A6-CYP2B6 locus were significantly associated in GWAS meta-analysis of the nicotine metabolite ratio [29]. SNPs in some GWAS-identified loci also influence susceptibility of developing smoking-related health outcomes, including: CHRNA5 with lung cancer (most recently [34]), lung function [35], airflow obstruction [36], COPD (most recently [37]), and peripheral arterial disease [9]; the nicotine metabolizing gene CYP2A6 with lung cancer [11], lung function [35], and
