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DNA sequence variants that decrease cholesteryl ester transfer protein (<jats:italic>CETP<\/jats:italic>) gene activity increase plasma HDL\u2010C; as such, medicines that inhibit CETP and raise HDL\u2010C are in clinical development. Here, we test the hypothesis that <jats:italic>CETP<\/jats:italic> DNA sequence variants associated with higher HDL\u2010C also increase risk for ICH.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We performed 2 candidate\u2010gene analyses of <jats:italic>CETP<\/jats:italic>. First, we tested individual <jats:italic>CETP<\/jats:italic> variants in a discovery cohort of 1,149 ICH cases and 1,238 controls from 3 studies, followed by replication in 1,625 cases and 1,845 controls from 5 studies. Second, we constructed a genetic risk score comprised of 7 independent variants at the <jats:italic>CETP<\/jats:italic> locus and tested this score for association with HDL\u2010C as well as ICH risk.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Twelve variants within <jats:italic>CETP<\/jats:italic> demonstrated nominal association with ICH, with the strongest association at the rs173539 locus (odds ratio [OR]\u2009=\u20091.25, standard error [SE]\u2009=\u20090.06, <jats:italic>p<\/jats:italic>\u2009=\u20096.0\u2009\u00d7\u200910<jats:sup>\u22124<\/jats:sup>) with no heterogeneity across studies (<jats:italic>I<\/jats:italic><jats:sup>2<\/jats:sup>\u2009=\u20090%). This association was replicated in patients of European ancestry (<jats:italic>p<\/jats:italic>\u2009=\u20090.03). A genetic score of <jats:italic>CETP<\/jats:italic> variants found to increase HDL\u2010C by \u223c2.85mg\/dl in the Global Lipids Genetics Consortium was strongly associated with ICH risk (OR\u2009=\u20091.86, SE\u2009=\u20090.13, <jats:italic>p<\/jats:italic>\u2009=\u20091.39\u2009\u00d7\u200910<jats:sup>\u22126<\/jats:sup>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>Genetic variants in <jats:italic>CETP<\/jats:italic> associated with increased HDL\u2010C raise the risk of ICH. Given ongoing therapeutic development in <jats:italic>CETP<\/jats:italic> inhibition and other HDL\u2010raising strategies, further exploration of potential adverse cerebrovascular outcomes may be warranted. Ann Neurol 2016;80:730\u2013740<\/jats:p><\/jats:sec>","DOI":"10.1002\/ana.24780","type":"journal-article","created":{"date-parts":[[2016,9,22]],"date-time":"2016-09-22T15:16:49Z","timestamp":1474557409000},"page":"730-740","source":"Crossref","is-referenced-by-count":40,"title":["Genetic variants in <i>CETP<\/i> increase risk of intracerebral hemorrhage"],"prefix":"10.1002","volume":"80","author":[{"given":"Christopher D.","family":"Anderson","sequence":"first","affiliation":[{"name":"Center for Human Genetic Research, Massachusetts General Hospital (MGH) Boston MA"},{"name":"J. Philip Kistler Stroke Research Center, Department of Neurology, MGH Boston MA"},{"name":"Division of Neurocritical Care and Emergency Neurology, Department of Neurology, MGH Boston MA"},{"name":"Program in Medical and Population Genetics, Broad Institute Cambridge MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guido J.","family":"Falcone","sequence":"additional","affiliation":[{"name":"Center for Human Genetic Research, Massachusetts General Hospital (MGH) Boston MA"},{"name":"J. Philip Kistler Stroke Research Center, Department of Neurology, MGH Boston MA"},{"name":"Division of Neurocritical Care and Emergency Neurology, Department of Neurology, MGH Boston MA"},{"name":"Program in Medical and Population Genetics, Broad Institute Cambridge MA"},{"name":"Departments of Epidemiology and Biostatistics, Harvard T. H. Chan School of Public Health Boston MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chia\u2010Ling","family":"Phuah","sequence":"additional","affiliation":[{"name":"Center for Human Genetic Research, Massachusetts General Hospital (MGH) Boston MA"},{"name":"J. Philip Kistler Stroke Research Center, Department of Neurology, MGH Boston MA"},{"name":"Division of Neurocritical Care and Emergency Neurology, Department of Neurology, MGH Boston MA"},{"name":"Program in Medical and Population Genetics, Broad Institute Cambridge MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Farid","family":"Radmanesh","sequence":"additional","affiliation":[{"name":"Center for Human Genetic Research, Massachusetts General Hospital (MGH) Boston MA"},{"name":"J. Philip Kistler Stroke Research Center, Department of Neurology, MGH Boston MA"},{"name":"Division of Neurocritical Care and Emergency Neurology, Department of Neurology, MGH Boston MA"},{"name":"Program in Medical and Population Genetics, Broad Institute Cambridge MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H. Bart","family":"Brouwers","sequence":"additional","affiliation":[{"name":"Center for Human Genetic Research, Massachusetts General Hospital (MGH) Boston MA"},{"name":"J. Philip Kistler Stroke Research Center, Department of Neurology, MGH Boston MA"},{"name":"Division of Neurocritical Care and Emergency Neurology, Department of Neurology, MGH Boston MA"},{"name":"Program in Medical and Population Genetics, Broad Institute Cambridge MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas W. K.","family":"Battey","sequence":"additional","affiliation":[{"name":"Center for Human Genetic Research, Massachusetts General Hospital (MGH) Boston MA"},{"name":"J. Philip Kistler Stroke Research Center, Department of Neurology, MGH Boston MA"},{"name":"Division of Neurocritical Care and Emergency Neurology, Department of Neurology, MGH Boston MA"},{"name":"Program in Medical and Population Genetics, Broad Institute Cambridge MA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alessandro","family":"Biffi","sequence":"additional","affiliation":[{"name":"Center for Human Genetic Research, Massachusetts General Hospital (MGH) Boston MA"},{"name":"J. 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