1994; Schuckit et al., 2004)), alcohol metabolism (Lind et al., 2008b; Martin et al., 1985a; Martin et al., 1985b), and alcohol craving (Anton, 1999; Mackillop et al., 2007, 2010; Monti et al., 2000; Sinha and O’Malley, 1999; Verheul et al., 1999). A detailed review of alcohol endophenotypes is presented elsewhere (Hines et al., 2005). Another approach to limiting heterogeneity has been the utilization of animal models and post-gene studies (i.e., transcriptome and proteome studies) to identify genetic factors related to specific components of alcoholism, such as alcohol consumption. For example, researchers have used whole-brain gene expression data of several mouse models of alcohol consumption to identify candidate genes and functional pathways related to voluntary alcohol consumption (Mulligan et al., 2006). By characterizing differences between mice that were never exposed to alcohol, but were characteristically known to differ in their levels of alcohol consumption, Mulligan et al. demonstrated that there are multitudes of neuronal pathways that differ between mice that are inherently destined to consume low/high amounts of alcohol. Likewise, there are many genes located within these pathways that are differentially expressed between these groups of mice because of variation within and among them. Notably, several of the 3800 unique genes
