the markedly lower AUD severity loadings are in subjects with insertions at chromosome 11 q14.2 suggests that insertions may have a positive influence on mitigating the effect of some behaviors or diseases. Similarly, deletion carriers in this region have significantly higher median loading coefficients. CNV deletions have previously been shown to have a general deleterious effect on variations in intelligence (Yeo, Gangestad, Gasparovic et al., 2011; Yeo, Gangestad, Liu et al., 2011) as well as autism risk (Pinto et al., 2010) and other neuropsychiatric diseases (Durand et al., 2007). The identified CNV region at chromosome 11 q14.2 corresponds to the ME3 gene malic enzyme which catalyzes malate to pyruvate and is involved in the glycolysis metabolic pathway. Several associations between ME3 malic enzyme 3 NADP(+)-dependent mitochondrial isoform and both schizophrenia and AIDS progression (Hendrickson et al., 2010; Martins-de-Souza et al., 2010) have recently been made. Similarly, polymorphisms in this gene have also been indicated as a factor in initiating tobacco use (Vink et al., 2009). This candidate region did not pass a Bonferroni corrected significance threshold. However, considering CNV’s relative infrequency (between 1 and 10%) in general populations (Kato et al., 2010), this is not surprising given the number of
