and in contrast to other GWAS for drug dependence, a number of other genes that had been previously associated with nicotine or drug dependence using candidate gene or genome-wide linkage approaches were apparent in this list including a number of nicotinic acetylcholine system genes, GABAergic genes, serotonergic system genes, opioidergic system genes and other neuropeptide associated genes. This is not true of comparison to drug dependence phenotypes as a whole and may represent specific contributions of these genes to nicotine dependence. A subsequent analysis of 3 nicotine cessation (quit-success) samples (G. R. Uhl, Liu, et al., 2008) identified a substantial overlap in the set of genes associated with nicotine cessation, and characterized by clustered positive SNPs. Once again, cell adhesion molecule genes were prominent in this analysis, along with genes coding for enzymes, transcriptional regulation and smaller numbers of genes associated with other functions, including some neurotransmitter receptors. As for most drug dependence GWAS (except perhaps nicotine dependence) monoamine system genes were conspicuous for their absence.
