were selected from both community-ascertained families and families with alcohol dependent probands, but could not share a common known ancestor with a case subject. Controls were required to have previously consumed alcohol, but not to have a diagnosis of alcohol dependence, abuse, or harmful use by any of the diagnostic systems included in SSAGA (Feighner, DSM-III-R, DSM-IV, and ICD-10). In addition, the controls could not have DSM-III-R or DSM-IV diagnoses of abuse or dependence for other substances (cocaine, marijuana, opioids, sedatives, or stimulants) to avoid potential genetic risk factors shared with alcohol abuse and dependence. Only the European–American subsample (N = 1399, 46.6% female) was used, to reduce population stratification. Genotyping was performed by the Center for Inherited Disease Research using the Illumina Infinium II assay protocol (Gunderson et al. 2006) with hybridization to Illumina HumanHap1M Bead-Chips (Illumina, San Diego, CA). Detailed information on genotyping can be found in Edenberg et al. (2010); data are available at dbGaP (phs000092.v1.p1). Symptom counts of AD, ASP, and MD were used as phenotypes for GWAS, and sex was used as a covariate. GWAS p-values of association between 989, 949 SNPs and each of the three phenotypes were computed using PLINK version 1.07 (Purcell
