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. 2023 Feb 15;25(6):1207–1211. doi: 10.1093/ntr/ntac268

Figure 1.

Figure 1.

Nicotine dependence severity did not mediate an association between the CYP2A6 wGRS and smoking cessation at end of treatment in the PNAT2 clinical trial. This model shows the relationship between the CYP2A6 weighted genetic risk score and smoking cessation success at end-of-treatment via nicotine dependence severity measured at baseline using FTND. The (a) pathway shows the association between the CYP2A6 wGRS and FTND score. The (b) pathways show the association between FTND score and smoking cessation success. The mediating effect of FTND on smoking cessation success is shown in the (a b) pathway (i.e. indirect effect pathway) and is shaded in dark gray. The (c) pathway shows the direct effect of the CYP2A6 wGRS on smoking cessation success adjusted for covariates, while the (cʹ) pathway shows the direct effect of the CYP2A6 wGRS on smoking cessation success adjusted for covariates and the indirect effect. Statistically significant effects (at p < .05) are bolded. Ancestry, sex, and age were included as covariates in the treatment-stratified analyses (n = 320 PLAC; n = 332 PATCH; n = 347 VAR). The overall analysis (n = 999) additionally controlled for treatment; results are shaded in light gray. Abbreviations: wGRS = weighted genetic risk score, FTND = Fagerström Test for Nicotine Dependence, OR = Odds Ratio, CI = confidence interval, PLAC = Placebo, VAR = Varenicline.