From the 48 genes implicated by at least two approaches, we prioritized likely causal genes for OCD using colocalization (TWAS-COLOC)27,28 and SMR–heterogeneity in dependent instruments (SMR-HEIDI)22 tests. Colocalization was used to identify significant TWAS associations for which the underlying GWAS and eQTL summary statistics are likely to share a single causal variant. Similarly, HEIDI was used to select SMR associations for which the same causal variant affects gene expression and trait variation. Of the 48 genes implicated by at least two gene-based tests, 25 were also significant in either the TWAS-COLOC or the SMR-HEIDI tests, suggesting causality (Fig. 2a). Only 2 of these 25 genes were prioritized by both TWAS-COLOC and SMR-HEIDI: WDR6 (WD repeat domain 6) and DALRD3 (DALR anticodon binding domain-containing 3). Another gene of interest, CTNND1 (catenin δ1), was implicated by three of our five approaches (multivariate set-based association test (mBAT-combo), TWAS, PWAS) and showed evidence for colocalization. Only three genes were implicated in the PWAS; of these, CTNND1 was the only gene also implicated in the TWAS. In the PWAS, downregulation of CTNND1 protein expression in
