We have performed the largest GWAS of schizophrenia to date and in doing so, identify a substantial increase in the number of associated loci. We show that genes we prioritise within associated loci by fine-mapping are enriched for those with an increased burden of rare deleterious mutations in schizophrenia, and identify GRIN2A, SP4, STAG1, and FAM120A as specific genes where the convergence of rare and common variant associations strongly supports their pathogenic role in the disorder. Importantly, this convergence also implies that the pathogenic relevance of altered function of these genes extends beyond the small proportion of cases carrying rare mutations. We also demonstrate that common variant schizophrenia associations are enriched at genes implicated in neurodevelopmental disorders, opening the door for using the increasing power of rare variant studies of those disorders to further prioritise genes from GWAS studies. Exploiting this, in addition to GRIN2A we identify BCL11B, CACNA1C, RERE, FOXP1, MYT1L and SLC39A8 as genes with strong support.
