These are not the only possible functional variants, and the explosion of the next-generation sequencing has uncovered a more comprehensive understanding of human genome variation, including at ADH1B. Considering the worldwide populations included in the 1,000 Genomes Project Phase 3 dataset (available at http://browser.1000genomes.org/index.html; [1000 Genomes Project Consortium and others 2015]), 145 missense variants have now been identified considering the canonical ADH1B transcript, but the total number of coding and non-coding variants is much higher, 1,110 SNPs (Supplemental Table 1). Non-coding variants may play very important roles in gene regulation, and consequently in the expression of phenotypic traits. Analyzing GTEx data (Release V6), we observed 165 independent ADH1B expression quantitative trait loci (eQTL) considering a false discovery rate (FDR) < 5% and a linkage disequilibrium (LD) r2 cutoff ≥ 0.1. These ADH1B eQTLs are related to 43 SNPs and 5 tissues, including subcutaneous adipose tissue, tibial artery, transformed fibroblast, tibial nerve, and thyroid (Supplemental Table 2). Considering multi-tissue eQTL posterior probabilities for ADH1B available in the GTEx dataset, rs10516440 showed effects on multiple tissues, including subcutaneous adipose tissue, tibial artery,
