Treutlein et al. (2009) recently reported results from a GWAS of German alcoholics. Their cases were male alcoholics who had been hospitalized for treatment or prevention of severe withdrawal. We had data for 114 of their top 140 SNPs (121 at p<10−4 in their study and 19 they nominated from rodent studies); 14 were significant in our primary analysis of alcohol dependence; 11 of these were also significant in our smaller subset of early-onset alcoholics (Table 4). Only one of these, rs13273672 in GATA4, was among the 15 SNPs for which Treutlein et al. reported confirmation in their follow-up (Treutlein et al., 2009). Among the SNPs for which we had replication, 6 have the same risk allele; these lie in or near ARL6IP5, ID4, GATA4, SYNE1, ADCY3 and PRKCA; three of these (GATA4, ADCY3, SYNE1) were among the top 6 with our early onset phenotype. These are all good candidate genes; two regulate transcription (ID4, GATA4), two (ADCY3, PRKCA) regulate important second messenger systems, one (ARL6IP5) inhibits the glutamate transporter EAAC1 and one (SYNE1) is associated with autosomal recessive spinocerebellar
