The Schizophrenia Exome Sequencing Meta-Analysis has sequenced roughly 88,000 people with schizophrenia and 150,000 without, and its second release names forty genes in which rare damaging variants raise risk substantially. Sixteen of those reach exome-wide significance; the other twenty-four pass a 5% false-discovery threshold. Gene-set analysis of the forty returns synapse, postsynapse, cell junction and glutamatergic synapse as the leading cellular components, which is the strongest evidence yet that schizophrenia risk converges on the synapse — though that convergence is a property of the set rather than of any one member, and seven of the sixteen strongest genes encode nuclear proteins. The gene set surveyed here is the sixteen exome-wide genes from that release. Credit for the genetics belongs to the SCHEMA consortium: Sealock, Dowd and colleagues, Analysis of rare coding variation identifies new genetic contributors to schizophrenia, bioRxiv 2026, doi:10.64898/2026.09.18.752670. What follows is a separate question: once the genetics has named a gene, what does the experimental literature already tell us about what losing it does?
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Adam Claridge‐Chang (2026) studied this question.
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