The existence of an underlying dimension of risk for drug dependence has the potential to be a useful tool for strengthening association studies, largely because it helps to refine the phenotype of interest. Evidence of a common liability for dependence implies that genetic variants involved have pleiotropic effects, which is understandable given that several neurobiological mechanisms and their genetic determinants have been associated with more than one substance. For instance, genetic variants in nicotinic acetylcholine receptor subunits have been associated with both tobacco and alcohol use (Ehringer et al., 2007; Schlaepfer et al., 2008a, 2008b) and the abolition of alcohol preference in mice is achievable through pharmacological targeting of the cannabinoid signaling system (Basavarajappa, 2007).
