In contrast, the proportion of TS variance explained was substantially lower (0.6%). Although some of the difference in polygenic risk prediction between OCD and TS may be due to the smaller discovery sample size for TS, a sensitivity analysis in which the OCD discovery sample size was reduced to match that of the TS sample (“Downsized OCD”), still detected a larger, and statistically significant, OCD polygenic signal than the comparable TS signal (p=0.01) (Figure 3, Table S3). The TS discovery sample was also too small to examine polygenic signals in TS subgroups (TS+OCD vs. TS-OCD); thus, it is possible that the TS polygenic signal could increase if “TS only” discovery and target samples were available. The TS polygenic signal may also have been attenuated by restricting polygenic risk score SNPs to those with MAF>5% (done to reduce bias due to undercalling of rare variants, see Supplementary Methods), as this class of SNPs has been shown to account for ~20% of the variance in liability to TS, with 80% attributable to common variants (10). Both the investigation of TS subgroups and
