Broadly speaking, there are at least three primary contexts in which genetic variation could influence liability for relapse during or following treatment. First, in the context of pharmacotherapy interventions, relevant genetic variations can impact drug pharmacokinetics or pharmacodynamics, thereby moderating treatment response (pharmacogenetics). Second, the likelihood of abstinence following a behavioral or pharmacological intervention can be moderated by genetic influences on metabolic processes, receptor activity/expression, and/or incentive value specific to the addictive substance in question. For instance, SNPs with functional implications for relevant neurotransmitter or metabolic pathways can influence the reward value of marijuana (e.g., FAAH; CNR1); nicotine (e.g., CYP2A6, CHRNB2, CHRNA4); and alcohol (ALDH2, ADH1B), while others show potential for influencing the incentive value of multiple drugs (e.g., ANKK1; DRD4; OPRM1). Third, variants implicated in broad traits relevant for addictive behaviors--for instance, executive cognitive functioning (e.g., COMT) or externalizing traits (e.g., GABRA2, DRD4)--could influence relapse proneness via general neurobehavioral mechanisms, irrespective of drug class or treatment modality. As summarized below, preliminary empirical support exists for each of these possibilities.
