We fully expect that future GWAS using larger sample sizes from expanded meta-analyses and large-scale biobanks with data on cigarette smoking, alcohol, and other drugs will identify and replicate additional loci with robust statistical evidence. These loci will likely include some variants that underlie specific addictions, while others are shared across different drugs of abuse and across psychiatric diseases that are highly co-morbid with addiction. This notion of shared genetic susceptibility is supported by schizophrenia-associated common genetic variation having significant correlations with smoking-associated genetic variation: for example, rg=0.14 for nicotine dependence, rg=0.12–0.14 for CPD, and rg=0.10 for ever/never smoking [121, 122]. Polygenic risk scores (weighted summations of top ranking subsets of genetic variant associations) have provided additional evidence for shared genetic etiologies. Polygenic risk scores based on GWAS-identified variants for schizophrenia or bipolar disorder have shown significant associations with smoking, alcohol, and substance use disorder phenotypes [123–125]. Early examples of genetic variants that demonstrate such pleiotropy, i.e., exert effects on more than one outcome, across addiction and other psychiatric diseases include: ZNF804A SNP rs1344706, the first genome-wide significant finding for
