Disease-associated markers both within and between genes can all begin to allow us to assess individual differences in vulnerability to addiction based on profiles of genotypes. In settings in which prevention of addiction is sought, addiction vulnerability genomic profiles could help to target more (or different) prevention resources to individuals at the most (or at different) genetic risk. When a therapeutic opiate is being considered for chronic, noncancer pain, for example, the costs of engendering substance dependence are likely to be sufficient to justify genotyping even if the results provide only partial information about risk assessment and minimization for prescribing physicians. When treatment for an established dependence on nicotine, opiates or alcohol is being contemplated, a number of different therapeutic options with different pharmacological mechanisms of action are now available [298]. Subsets of the SNPs that we have associated with success in quitting smoking appear to provide selective influence success in responding to bupropion, while others appear to provide selective influences on success in response to nicotine replacement. Replication and extension of these observations to treatments for alcohol, opiates and
