resistance to alcohol dependence, but to date, no subsequent work has been published on these polymorphisms as regards alcohol dependence. In addition to these, another CNR1 SNP (rs202323) has been implicated in mediating cue-reactivity to alcohol in heavy drinkers, where individuals with at least one copy of the C allele display increased craving and salivary response to an ethanol associated cue (van den Wildenberg et al., 2007). A follow up to this study found that the C allele was correlated with increased CB1 expression in post-mortem samples of human PFC, and alcohol dependent patients with the C allele had increased activation in the PFC, orbitofrontal cortex, and NAc in response to ethanol-associated cues (Hutchison et al., 2008). These individuals also reported increased sensation of reward and positive affect following consumption of several alcoholic beverages, suggesting the C allele may confer increased likelihood of binge ethanol use. These results suggest that genetic variation in the CNR1 may contribute susceptibility to the development of AUDs, but future studies are needed to confirm and extend the data regarding the role these SNPs play in alcohol dependence.