The genetic association studies so far have shown that the genes that may contribute to variation in the risk for addiction are not specific to a drug (e.g., rev. in Li and Burmeister, 2009). In some contrast to known or expected associations for the risk for disorders related to licit compounds (alcoholism and tobacco dependence; ADH and ALDH genes and CYP2B6 and CHRNA group genes), those related to illicit drugs point to dopamine, serotonin and GABA receptor and/or transporter and other non-drug-specific genes involved in neurotransmission and neurobiology (e.g., BDNF, ANKK1 and NRXN1). Even the connections of the nicotinic acetylcholine receptor genes, however, originally observed for nicotine dependence, have now been extended to cocaine and opiate dependence, sometimes with flip-flops of alleles specifically associated with the licit and illicit substances (Sherva et al., 2010). Associations with CLA may be also expected for genes that are part of the mechanisms of neural plasticity, potentially involved in reaction to all external stimuli including (nonspecific) drug response. Such mechanisms likely include, for instance, epigenetic regulation, e.g., histone acetylation, which appears to participate in
