COGA was initiated as a linkage study with microsatellite markers, and subsequently genotyped variants in genes encompassed by these linkage regions. With the advent of genome‐wide association study (GWAS) arrays, several periods of funding secured GWAS genotyping of a majority of the sample (4. Genetics). Other genomic data in COGA include a small subset of families with whole exome sequence data as well as whole genome methylation data on a subset of youth who transitioned to heavy episodic drinking. However, our analytic focus remains on the fuller GWAS dataset (4. Genetics) which contributed to some of the first GWAS of AUD. 42 , 43 The contribution of COGA data to meta‐analyses ultimately yielded the sample sizes necessary to identify credible loci for AUD and problem drinking, 5 , 6 however the deep phenotyping of COGA has also allowed us to discover variants associated with individual alcohol dependence criteria, criterion‐count based severity, 44 subjective ratings of ethanol, 45 drug dependence, 46 maximum drinks, 47 as well as brain function phenotypes. We have also utilized polygenic scores (PGS, or polygenic risk scores,
