In a similar vein, our comparison of all genes mapping within rare TS CNVs to genes previously implicated in ID, ASD, and SCZ support the hypothesis of shared genetic risks, but only for ASD and TS (Table 2, Figure 2). Consistent with this, several case reports and cohort studies point to an increased rate of comorbidity between ASD and TS or tic disorders (68-72). A prior genome-wide CNV study of TS (48) supported this finding and also suggested a convergence of risks among TS and SCZ as well. We did not find evidence for the latter. However, it is important to note that the previous study did not have a sufficient number of observations to conduct a meaningful statistical analysis and, conversely, our study did indeed find genes within TS CNVs that have previously been identified as putative SCZ risks, including CNTNAP2 and ASTN2 (Tables 2 and 3). As we did not have comprehensive phenotypic data regarding social disability syndromes or psychosis in our TS cohort, it was not possible for us to assess phenotypic overlap in individuals with putatively