respectively, highlighting a role for these neurons in AUD. In the future, AUD‐associated variants identified by COGA will be modeled in iPSC‐derived neurons using methods to selectively manipulate the expression of the gene of interest in a controlled genetic environment. In addition, PGS can be modeled in populations of iPSC‐derived neurons to search for pathways that could be linked with responses to alcohol. These examples, starting with genes or loci associated with AUD, followed by the evaluation of their functional consequences in human neuronal models from COGA participants, and the correlation of those findings with the rich phenotypic data from the same participants, demonstrate that the deep integration of multimodal data within COGA enables functional studies to reveal mechanisms linking genomic variants with AUD.
