Convergences between rare variants and fine-mapped GWAS signals have been previously observed in other traits e.g.,34,35, suggesting that genes most strongly implicated by fine-mapping and which have additional support from rare variant data are compelling candidates. Of the 10 exome-wide significant genes identified by SCHEMA36, two were prioritised candidates from fine-mapping; GRIN2A encoding a glutamatergic NMDA receptor subunit, and SP4, a transcription factor highly expressed in brain and which is regulated by NMDA transmission, and also regulates NMDA receptor abundance37. Two other genes supported by SCHEMA at FDR<0.05 had strong support from fine-mapping: STAG1, which is involved in controlling chromosome segregation and regulating gene expression, and FAM120A, which encodes an RNA binding protein. SNPs mapping to these genes had cumulative FINEMAP PP of 0.88 and 0.72 respectively (Supplementary Table 11b). The prioritised fine-mapped set also contained 4 genes implicated in DD; a transcriptional regulator (BCL11B), the well-known CACNA1C38, and genes mentioned elsewhere in this paper (GRIN2A and SLC39A8). Genes encoding additional transcriptional regulators are also of note; RERE, FOXP1 and MYT1L. RERE was prioritised by SMR and is associated with
