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Genome\u2010wide linkage studies and genome\u2010wide association studies in European ancestry cases identified over 50 vitiligo susceptibility loci, defining a model of melanocyte\u2010directed autoimmunity. Vitiligo heritability is exceedingly high, ~2\/3 coming from common and ~1\/3 from rare genomic variants; ~20% of vitiligo risk is environmental. Vitiligo genetic risk is polygenic, with greater additive risk in multiplex vitiligo families than simplex cases. Vitiligo age\u2010of\u2010onset is bimodal, also involving a major genetic component; a MHC enhancer haplotype confers extreme risk for vitiligo (OR 8.1) and early disease onset, increasing expression of <jats:italic>HLA\u2010DQB1<\/jats:italic> mRNA and HLA\u2010DQ protein and thus perhaps facilitating presentation of triggering antigens. Vitiligo triggering also involves a major environmental component; dramatic delay in vitiligo age\u2010of\u2010onset, especially from 1973 to 2004, suggests that exposure or response to a key vitiligo environmental trigger diminished during this period. Together, these findings provide deep understanding of vitiligo pathogenesis and genetic architecture, suggesting that vitiligo represents a tractable model for investigating complex disease genetic architecture and predictive aspects of personalized medicine.<\/jats:p>","DOI":"10.1111\/pcmr.12848","type":"journal-article","created":{"date-parts":[[2019,11,19]],"date-time":"2019-11-19T19:21:33Z","timestamp":1574191293000},"page":"8-15","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":67,"title":["The genetic architecture of vitiligo"],"prefix":"10.1111","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4007-0700","authenticated-orcid":false,"given":"Genevieve H. 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