Surprisingly, while twin studies suggested substantial shared genetic liability across multiple SUDs, the first GWAS of alcohol and nicotine phenotypes, including their problematic use, identified missense variants in genes that encode substance-specific metabolizing enzymes or neurotransmitter mechanisms (e.g., rs1229984 in ADH1B [encoding alcohol dehydrogenase 1B] for alcohol dependence; rs16969968 in CHRNA5 [encoding the α5 subunit of a nicotinic acetylcholine receptor] for nicotine phenotypes) (66–69). This evidence concerns the gene ADH1B and alcohol dependence.