including chromosome regions have been identified by overlapping genetic linkage and functional data with alcoholism-related phenotypes of interest and refined to develop a molecular signature of alcoholism phenotype (Ehlers et al., 2004; Enoch, 2013; Kapoor et al., 2014; Wetherill et al., 2014). A representative example of a candidate gene/biomarker analysis is the alcohol dehydrogenase enzyme (ADH) which is responsible for alcohol metabolism and linked to the ADH gene family located in the 4q23 chromosome band (Chai et al., 2005; Edenberg et al., 2006; Macgregor et al., 2009; Tolstrup et al., 2008). The 4q23 chromosome band has been strongly associated with alcoholism vulnerability in several genome-wide linkage studies (Long et al., 1998; Reich et al., 1998). The activity of alcohol metabolizing enzymes (e.g., ADH) influences sensitivity to alcohol, its effects on the body and the accumulation of metabolites (e.g., acetaldehyde) which may be toxic. Genetic variants that increase production or slow the processing of alcohol intermediates (e.g., ADH1B, ADH1C, ALDH2) influence the likelihood of developing a drinking problem (Chai et al., 2005; Edenberg et al., 2006; Macgregor et al., 2009; Tolstrup et al., 2008). Human genetic studies have similarly identified alcoholism candidate genes involving neurotransmitter pathways associated with brain reward processes
