with higher monitoring increased to 4.08 with low parent monitoring. In men, OR for risk genotype =2.03 with higher monitoring increased to 2.76 with low parent monitoring. However, there is a potential gender difference in the interaction between lowest quartile parent monitoring and risk genotype of rs16969968, which may be beyond the statistical power of the current study sample. However, there are many more environmental and personal risk factors (e.g., childhood adversity, peer use, parental smoking, and personality characteristics) as well as specific genes what influence the development of nicotine dependence than were examined here (43–46). The variance (r2) explained by these two SNPs and parent monitoring is 4.2%. We anticipate the discovery of many more genetic and environmental risks associated with the development of nicotine dependence. More complex and complete models will need to be developed in the future. Another limitation is the ascertainment bias. The estimation of gender-specific prevalence of nicotine dependence needs to take into account the ascertainment bias. However, we were able to control for the potential confounding effects of gender in our study when examining the association between genetic/environmental risks and nicotine dependence in multivariate regression models. Caution is needed in interpreting our findings on
