The fine mapping analysis of all 171 GWAS loci pinpointed putatively causal variants with high resolution in some cases. The 95% credible interval for 34% of the loci had <10 SNPs and 24 loci had double basepair resolution, including several instances where the sole putative causal variant was nonsynonymous and of lower frequency, although in only one case with MAF<1%. The resolution increased somewhat when functional information was used to inform the prior, with double base-pair resolution at 32 loci, and 44% of loci having <10 SNPs in the 95% credible interval. Table 1 includes all nonsynonymous or loss of function variants within the genome-wide significant loci that had a posterior probability of association greater than .80 from at least one of the fine mapping methods. Additional results from the fine mapping analysis are available in Tables S6 and S7. Several known functional variants were identified through this method, including: rs16969968(56), a nonsynonymous variant in nicotinic receptor gene CHRNA5 associated with CigDay (PPA=.92 and .84 from the fine mapping analysis with, and without, functional priors, respectively); rs1229984(57), a nonsynonymous variant
