In conclusion, although our findings were derived from a relatively small sample compared to those used for GWAS of other complex psychiatric diseases, we identified significant associations in genes never before implicated in SUD risk, one of which, in contrast to the top findings from published dependence diagnosis GWAS papers, showed evidence for association in both AA and EA ancestry groups. Although the effect size is small and the effect of the variant has little if any implication for the prediction or treatment of SUDs, it may point to a novel SUD-relevant pathway. Measuring gene and gene network expression changes after perturbing FAM78B in cell lines or mouse models would be a logical next step to determine if such a pathway exists. This work also highlights the value of analyzing related phenotypes for addictive disorders given the scarcity of risk genes identified through dependence diagnosis GWAS.
