associated with a phenotype), along with the “hidden heritability” (the difference between heritability estimated using all the SNPs on a genotyping chip, known as h 2 SNP, and h 2 GWAS) and “still‐missing heritability” (the difference between h 2 family and h 2 SNP). 110 , 111 , 112 , 113 AUD and other alcohol‐related traits are no exception: while the family‐based estimates of AUD heritability range from 50% to 64%, current SNP‐based methods estimate the heritability of AUD to be around 7%–10%. 7 This difference reflects, in part, that GWAS chips tag common but not rare variants. The family‐based nature of COGA enables exploration into the still‐missing heritability. For example, a method from Zaitlen et al. 114 allows the joint estimation of pedigree heritability (h 2 family) and SNP‐heritability (h 2 SNP) in the same model in samples of related individuals, such as COGA. The presence of both close and distant relatives in COGA might also enable exploration of potential causes for inflated twin‐based heritability estimates, including shared environment, dominance effects, and epistatic interactions. Furthermore, dense family pedigrees, such as those found in COGA, provide a unique resource for identifying rare variants associated with AUD and related traits, which
