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 where the underlying GWAS and eQTL summary statistics are likely to share a single causal variant. Similarly, HEIDI was used to select SMR associations where the same causal variant affects gene expression and trait variation. 25 of the 48 genes implicated by at least two gene-based tests were also significant in either the TWAS-COLOC or SMR-HEIDI tests, implying causality (Fig. 2a). Only two of these 25 genes were prioritized by both TWAS-COLOC and SMR-HEIDI, WD repeat domain 6 (WDR6) and DALR Anticodon Binding Domain Containing 3 (DALRD3). Another gene of interest, Catenin Delta 1 (CTNND1), was implicated by three of our five approaches (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 human dorsolateral prefrontal cortex was
