While the original QTL mapping work was nearly all based on linkage and association analysis of numerous polymorphisms across the genome, the use of DNA chips and microarray analyses to identify QTLs was soon adopted. Differences in gene expression have therefore also helped to identify the specific genes in these and other regions in both mice and rats that may be responsible for differences in ethanol consumption (Carr et al. 2007; Hitzemann et al. 2004; Mulligan et al. 2006; Tabakoff et al. 2008; Treadwell et al. 2004; Weng et al. 2009a, b; Worst et al. 2005). Gene sequence data have also been examined (Fehr et al. 2005; Boyle and Gill 2008). To date, none of the evidence can be considered definitive with regard to concluding that a gene accounting for differences in ethanol consumption has been identified. However, compelling candidates include syntaxin binding protein 1 (Stxbp1) on chromosome 2 and sodium channel, type IV, (Scn4b) on chromosome 9, among many others, including some mentioned above. A significant development corresponding with the ability to examine the expression of thousands of genes
