Results are inconsistent for CNR1, GABRA2, FAAH, and ABCB1 (Benyamina et al., 2009; Haughey, Marshall, Schacht, Louis, & Hutchison, 2008a; Lind et al., 2008b; Verweij et al., 2012) and as such require additional investigation. Both CNR1 and FAAH have been associated with phenotypes related to reward sensitivity, impulsivity, and negative affect. Further, additive gene-gene interactions between FAAH (C385A; rs324420) and CNR1 (rs2023239) have been associated with cue reactivity as defined by negative affect during cannabis abstinence (Filbey, Schacht, Myers, Chavez, & Hutchison, 2010; H. M. Haughey, et al., 2008a). CNR1 encodes a presynaptic cannabinoid 1 receptor with dense expression in regions related to reward, addiction, and cognitive function; i.e., amygdala, cingulate cortex, prefrontal cortex, ventral pallidum, caudate putamen, nucleus accumbens, ventral tegmental area, and lateral hypothalamus, (Glass, Faull, & Dragunow, 1997; Wang, Dow-Edwards, Keller, & Hurd, 2003). ABCB1 (adenosine triphosphate-binding cassette subfamily B member 1) is responsible for P-glycoprotein production. P-glycoprotein has been studied for its role in drug pharmacokintetics because it is present in endothelial cells of the blood-brain barrier which limits accumulation of its substates in the central
