The primary mechanism of cocaine is blockade of monoamine transporters, and the rewarding properities of cocaine are predomeintly associated with blockade of cell surface dopamine transporters. Thus, cocaine increases dopamine levels in the synaptic cleft by decreasing reuptake (Kiyatkin, 1994; Wise, 1984). Consequently, many genetic association studies of cocaine use disorder focus on genes whose products function in the dopaminergic pathway including genes whose products are responsible for D2 dopamine receptor (DRD2) expression, dopamine signalling regulation (ankyrin repeat and kinase domain containing 1, ANKK1 and tetratricopeptide repeat domain 12, TTC12), dopamine metabolism (dopamine beta-hydroxylase, DBH; (Kaufman & Friedman, 1965; Weinshilboum, 1978) and degradation (catechol-O-methyltransferase, COMT), termination of dopamine transmission across the synapse (solute carrier family 6 member 3, SLC6A3 and NCAM1), and dopamine synthesis (tyrosine hydroxlylase, TH; (Bi, Gelernter, Sun, & Kranzler, 2014; Dahl et al., 2006; Farrer et al., 2009; Gelernter et al., 2006; Grucza et al., 2008; Ittiwut et al., 2011; Kalayasiri et al., 2007; Levran et al., 2015; Luo et al., 2004; Malison et al., 2006; Sherva et al., 2010; Zhang et al., 2009; Zuo et al.,
