Studies of twins suggest that genetic differences between individuals play an important role in smoking behavior, cessation, and in response to anti-smoking interventions.6 Recent genome-wide association studies (GWAS) in adult smokers and former smokers revealed genes that relate with genome-wide significance to smoking quantity (number of cigarettes smoked per day).7-9 These genes are already being used in clinical applications; e.g., to predict smoking cessation likelihood and in pharmacogenetic analyses.10-14 An important additional step in the translation of these GWAS findings is to test if genetic markers that predicted smoking quantity in GWAS also predict the development of smoking behavior in adolescence.15,16 This question is of critical importance for public health practice as intervention to disrupt genetic risk is likely to be most effective early in the development of dependence. Important developmental phenotypes in the pathogenesis of adult dependence include smoking initiation, conversion to daily smoking during adolescence, and rapid progression to heavy smoking.17 Early, rapid progression from smoking initiation to heavy use is a signal risk for adult nicotine dependence.18-21 Therefore, the present study tested relations of GWAS-identified genetic risk
