In 1996, the first gene-targeted mouse to be tested for alcohol preference drinking was found to drink more than it's wild-type counterpart, suggesting that the serotonin 1B receptor gene might play a role in preference drinking (Crabbe et al. 1996). However, several subsequent studies showed that this single gene effect was strongly dependent on the genetic background of the mice, and we have not to date been able to ascertain the physiological basis of the role of this gene in drinking (Phillips et al. 1999; Phillips and Belknap 2002; Crabbe et al. 1999). Since then, many additional over expression or null mutants have been created and tested for alcohol preference drinking. In 2006, we reviewed results for 76 targeted genes (Crabbe et al. 2006). Since that review, mutants for at least 10 additional genes have been tested. The review covered standard gene knockouts, over expression transgenics, and targeted point mutations, most expressed throughout development but some altered conditionally or in a brain region specific manner. These various manipulations of 23 genes increased preference drinking significantly; for 30 genes, preference was
