The first candidate gene we examined was the cannabinoid receptor 1 gene (CNR1). A report by Zhang and colleagues [36] suggests that an intronic single nucleotide polymorphism (SNP) (rs2023239) may create an alternative CNR1 transcript in the brain and suggests that this SNP and two others are associated with substance abuse in general. However, a recent study conducted by Herman and colleagues [37] failed to replicate these findings in both European American and African American populations with a primary diagnosis of alcohol dependence. The second candidate gene chosen for investigation was the fatty acid amide hydrolase gene (FAAH). Previous studies have demonstrated that the fatty acid amide hydrolase (FAAH), the enzyme that metabolizes Δ9-tetrahydrocannabinol (THC) in the brain, is a critical temporal regulator of endocannabinoid signaling [38–40]. One SNP in FAAH of interest (rs324420) involves a non-synonomous 385C to A substitution that converts a conserved proline residue to threonine. A previous study found an association between this SNP and substance abuse [38]. Although the functional significance of this non-synonomous SNP is not understood fully, the 385A variant encodes for a
