Twin and family studies have repeatedly demonstrated that TS is highly heritable.8 First-degree relatives of affected individuals have a 5-15-fold increased risk of TS compared to that of the general population, representing one of the highest familial recurrence risks among common neuropsychiatric diseases.3, 9 However, despite this strong familiality, identification of TS susceptibility genes has been challenging. Linkage analyses have produced inconsistent results, although a recent study combining multi-generational families with affected sibling pairs has identified at least one major TS locus on chromosome 2p.10 Multiple candidate genes have also been proposed, although none have been consistently replicated.8 Mutations in the strongest TS candidate genes (SLITRK1, CNTNAP2, and HDC) have been found only in single families or a small number of individuals, suggesting that, if truly causative, they account for only a small proportion of TS cases.11-15 Thus, additional gene-finding strategies are needed. Here, we report the first TS GWAS in a large cohort of samples of general European ancestry, as well as two European-derived population isolates, Ashkenazi Jews from the US and Israel (AJ) and French Canadians from Quebec,
