and decreased ethanol drinking (Hodge et al., 1999). Not all gene-targeted mouse studies, however, show this inverse relationship. In an extensive review of the subject, Crabbe et al. found that 19 out of 48 (40%) genes studied showed opposite effects on ethanol consumption vs. acute sedation, but 12% showed increases in both traits and another 48% were equivocal (Crabbe et al., 2006). These studies thus indicate that acute level of response to ethanol often, but not always, has predictive value for identifying molecular events relevant to ethanol consumption including long-term ethanol drinking behavior in humans. The studies on Clic in this report document a novel gene affecting the acute level of response to ethanol across multiple species, and thus could have important implications for understanding the mechanisms that affect ethanol consumption.
