due to incomplete matching during QC or other, unknown, technical biases, as all cases were genotyped with identical technology, shared the same control set, and were imputed together. Taken together, these results advance our understanding of the overlapping and non-overlapping genomic architectures of TS and OCD and suggest that non-overlapping elements of the architecture of each phenotype may be a limiting factor in the genetic relationship between them. Moreover, these results may be used to inform priorities for future studies of both disorders. For example, given the apparent contribution of rare variants to the heritability of TS, DNA sequencing may be a particularly informative analysis, whereas larger sample sizes and additional GWAS is likely to identify the majority of susceptibility variants for both disorders. Future studies aimed at understanding the genetic control of shared neurocircuitry in TS and OCD may be most well powered by testing the association of shared genetic risk (i.e., common polygenic brain eQTLs) with a well-defined quantitative neurobiological endophenotype. Studies such as the one presented here continue to highlight the value of “big picture” analyses, which provide insight into the genetic landscape of a phenotype, as a necessary and intelligent complement to the mapping of specific
