CNVs are duplications or deletions of a particular segment of an individual’s genome and reflect inherent structural instability in the architecture of the genome. They are prevalent forms of common genetic variation and can have a substantial influence on gene expression levels (Perry et al., 2007). For instance, Mendelian disorders such as Williams-Beuren Syndrome (due to a deletion at chromosome region 7q11.23) and Charcot-Marie-Tooth neuropathy Type 1A (caused by duplication at chromosome region 17p11.2 (Krajewski et al., 2000; Martens et al., 2008) are attributable to CNVs. Despite the deleterious effects of CNVs and their links to disease, few studies have examined CNVs in the context of psychiatric illness, particularly alcohol dependence. This is primarily due to the inherent challenges involved in identification of what constitutes a CNV. While traditional methods of CNV identification involve laboratory-based experiments, they can also be identified (or “called”) using GWAS data where a series of single nucleotide polymorphisms (SNPs) or “intensity” probes are interrogated for their occurrence in a state other than the expected disomic (i.e. 2 copy) state. Typically, the intensity of the probe
