Despite a significant boost in the number of genome-wide significant loci, variants identified in these large GWASs still explain a very small proportion of estimated genetic effect (heritability) for AUD and alcohol consumption. The SNP heritability estimates of AUDIT-C scores for all loci in MVP and the meta-analysis of the UKBiobank and 23andMe data ranged from 0.6 to 8 percent respectively[61, 62]. Heritability estimates for AUD were slightly lower and ranged from 0.5 to 5.9 percent in MVP versus UKBiobank and 23andMe meta-analysis respectively[61, 62]. These estimates are still significantly lower than the heritability estimates of AUD from twin and family studies. Given the heterogeneity in the diagnosis and polygenicity of this complex trait it seems that we are still short of required sample size to identify all the variants associated with disease. Some researchers working with other complex psychiatric traits argued that missing heritability can be explained by rare to low frequency variants of relatively large effect sizes. These rare variants can be identified by next generation sequencing in large cohorts. Contrary to expectations, recent sequencing studies for neurological
