There has been enormous progress in SUD genetics research towards the goal of understanding the molecular risk factors for SUDs, mostly in the past few years. For those traits that are well-represented in biobanks, such as alcohol and tobacco use traits, the prospects are very good for continued progress, discovery of more risk loci, and improvement in our knowledge of their biology. The prospects are not quite so good for illegal SUDs that tend to be less-well-represented in biobanks. For these traits, we will need directed recruitment as well as biobank data. Biobanks have both strengths and weaknesses for discovery. For less-prevelent or stigmatized traits, even large biobank samples may not provide sufficient information to investigate SUD polygenic architecture adequately. A further limitation of EHR data and some biobank assessments is that they meaure state rather than trait, whereas we are generally more interested in lifetime diagnoses than the research participant’s characteristics at a specific point in time. As recently shown181, alcohol consumption, tobacco smoking, and phenotyping of other traits are subject to misreports and longitudinal changes, causing biases in
