and standardized the adjusted phenotype by rank-based inverse-normal transformation. The GWAS analyses were performed in BOLT-LMM58 using all 7.3 million SNPs with a subset of 0.7 million SNPs in common with HapMap359 used to control for population structure and polygenic effects. We used self-reported “ever-smoked” as a dichotomous phenotype for smoking (208,988 cases and 244,705 controls). We analyzed the data in BOLT-LMM based a linear model with age and sex fitted as covariates, and transformed the effect size of each SNP on the observed 0–1 scale to odds ratio (OR) using LMOR60 (URLs).
