those important in nicotine addiction or smoking cessation, including gap junction, LTP, and MAPK signaling (Li 2008). These findings suggest that some but not all of the mechanisms underlying nicotine dependence are common with other substances in addiction. There are likely many genetic targets in other neuronal pathways that affect smoking behavior (Munafo and Johnstone 2008); therefore a pathway-based approach may be restricted by the large number of genes that contribute to other disease phenotypes and those for which a biological function is still unknown (Elbers et al. 2009; Munafo and Johnstone 2008; Wei et al. 2010). A pathway-based approach may help in the interpretation of genome-wide association data and lead to identification of novel mechanisms and genes contributing to smoking behavior (Wang et al. 2007; Wang and Li 2010).
