family and case control genome-wide efforts met with similar fate of limited success and non replication across different studies[52, 55]. At this point in time researchers already realized that AUD is highly polygenic and sample size of individual cohort is not enough to identify the SNPs with very small effect sizes[28]. Availability of raw genotype data through dbGAP also made it a bit easier to meta-analyze the similarity ascertained cohorts with genome-wide SNP data. Schumann and colleagues[56] meta-analyzed 26,316 population based subjects and a follow-up sample of 21,185 EA subjects and identified variants in the autism susceptibility candidate 2 (AUTS2) gene significantly associated with alcohol consumption (gms/ day/ kg of body weight). Subsequently, Kapoor and colleagues[49] meta-analyzed two large complementary and well-characterized EA cohorts assessed using the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) and identified rs1229984 SNP in ADH1B to be genome-wide significantly associated with phenotype measuring maximum number of alcoholic drinks in 24 hour. This was the first alcoholism related GWAS that reported genome-wide significance at this locus[49].
