Common forms of genetic variation, like single nucleotide polymorphisms (SNPs; individual DNA variants), account for a modest amount of variance in AUD11,12. AUD is polygenic and shares genetic risk with other substance use traits13. Outside of putative alcohol metabolism genes and neurotransmission genes, the biological basis of the genetic predisposition to AUD or problematic alcohol use remains elusive. One important mediator of genetic risk could be neuromolecular events as DNA variation has been shown to predict differentially expressed genes linked to AUD in addiction neurocircuitry14. How, or whether, alternative mRNA splicing mediates the genetic risk to AUD is unknown.
