While our previous work in this sample provides evidence of genetic sharing between TS and OCD, with a genetic correlation of 0.41 between the two disorders (10), we did not identify any genome-wide significant variants for the combined TS/OCD phenotype in this GWAS analysis, despite the increase in sample size. However, the combined GWAS signals were significantly enriched for functional alleles (parietal eQTLs), suggesting that these subthreshold variants contain some proportion of TS/OCD risk loci that are not simply due to stochastic variation. In the presence of genetic heterogeneity (see below), the current sample is underpowered to determine whether these loci contribute to both TS and OCD susceptibility, or to one or the other individually. As with any genetic association result, replication in an independent sample is required to know whether any of the individual eQTLs identified here are truly shared TS/OCD susceptibility variants (9, 26, 27).
