Although genetic variation influences the development of NicW, few risk genes have been identified.19–22 The identification of risk genes could provide insight into the molecular mechanism of NicW in humans. We conducted a genome-wide association study (GWAS) of DSM-IV NicW in a combined sample of 8021 European American (EA) and African American (AA) tobacco smokers. The sample was recruited for studies on the genetics of cocaine, opioid, and alcohol dependence (Yale-Penn study),23–25 and was augmented with GWAS data from subjects in the Study of Addiction: Genetics and Environment (SAGE), which are available to researchers through dbGAP (Database of Genotypes and Phenotypes).26–28 We previously published a GWAS of FTND score that was based partially on this dataset.29
