Alcohol dependence (AD) is a common and debilitating disorder, and ranks among the leading causes of the global burden of disease (World Health Organization 2009). Despite extensive research, it is unclear why only a proportion of all individuals exposed to alcohol become addicted. Elucidation of this point is important for the development of successful prevention and treatment strategies for AD. Previous research has shown that susceptibility to AD is partly genetic, and has a heritability of 40–60% (Enoch & Goldman 2002). The introduction of high-density SNP chips has enabled the systematic investigation of common variation in the human genome, and a large number of genome-wide association studies (GWAS) for a wide range of complex disorders have been published to date (Hindorff, Junkins, Hall et al. 2010). These investigations have implicated new variants, genes, and pathways. However, they have also demonstrated that sample size is crucial in detecting findings with genome-wide significance due to a combination of two effects. Firstly, effects of individual (common) variants are typically rather small and, secondly, as a consequence of the large number of simultaneously investigated
