While a better understanding of the genetic epidemiology of SUD is expected to reduce its burden on society, prevention has been very successful particularly for reducing rates of population-level drug use. For example, changes in policy and expectations in the social norms related to substance use have reduced the prevalence of smoking initiation in the United States (Do & Maes, 2016). To date, it is unclear how genetic variants influence these outcomes and subsequently translate into successful treatment and prevention of relapse among those with nicotine dependence (Hutchison, 2010). Nonetheless, there are several exciting possibilities for further exploration, as twin studies have reported that additive genetic influences account for 11%–74% of the variance of smoking abstinence (Broms, Silventoinen, Madden, Heath, & Kaprio, 2006; Heath, Madden, & Martin, 1998; Heath & Martin, 1993; Heath, Martin, Lynskey, Todorov, & Madden, 2002; J. Kaprio, Koskenvuo, & Sarna, 1981; Madden et al., 1999; Medlund, Cederlof, Floderus-Myrhed, Friberg, & Sorensen, 1976; True et al., 1997). Moreover, several genetic polymorphisms have also been found to impact therapeutic effectiveness for nicotine use disorders (Colilla et al., 2005;
