between CHRNA4, nicotine dependence, a “rush” or “high” following a cigarette, and the expression of α4β2 nAChRs in the nucleus accumbens. This study also presented functional data for two SNPs in the 5′UTR and promoter region of CHRNA4. Two other studies focused on CHRNB2 failed to find evidence for an association with nicotine phenotypes (Lueders et al., 2002; Silverman et al., 2000). However, a more recent study found evidence for an association between age of initiation of smoking in women and CHRNB2 (Greenbaum et al., 2006). Furthermore, our group found evidence for association between a rare SNP in the 5′UTR of CHRNB2 (rs2072658) and early subjective response to both alcohol and tobacco as well as modest evidence for association between past six month alcohol use and CHRNA4 (Ehringer et al., 2007). In the current study, significance levels for CHRNA4 are comparable to those for CHRNB3, but since this gene was not tested as an a priori hypothesis the experiment-wide empirical p-values did not meet significance. Although we did not detect an association with CHRNB2 in this study, only four SNPs (not including rs2072658) were genotyped, so it is possible this gene was not fully saturated. Since α4 and β2 subunits
