may have impacted our PGSAUD analyses in COGA and Indiana Biobank, if, for instance, our regression missed a specifically influential confounder. Environmental influences and psychiatric comorbidities, as well as their interactions with genetic factors are also significant contributors to AUD. Assessing risk for AUDs is therefore complex, with many potential gene-environment interactions that can mitigate the influence of high genetic risk or amplify the influence of low genetic risk. Therefore, PGSAUD alone, absent a broader assessment of risk, could easily be mis-interpreted to determine the need for treatment while ignoring other important factors in the development of AUD (de Hemptinne and Posthuma, 2023). However, while there is the potential to misuse genetic information, we believe that the potential benefits are much greater as it is a common clinical practice to escalate care for those identified to be at greater risk. It is our hope that eventually PGSAUD can be used in combination with behavioral or other assessments and family history to provide timely and effective treatment for those in the early stages of AUD before they progress to severe AUD and related health conditions.
