The clearest published answer to "how many genes?" for any psychiatric condition: about 8,300 of them, together explaining at least a third of the liability. Which is also why no single one of the fourteen on this page tells you anything.
Solid lines are connections this site curates. Dashed lines mean the two ends share a research paper — worth knowing, and not a claim that one explains the other.
Schizophrenia is a psychiatric illness of altered perception and thought — hallucinations, delusions, disorganised thinking — usually beginning in late adolescence or early adulthood. It affects roughly 1 in 100 people over a lifetime and has been recognised as a distinct condition for over a century, without a biological marker to define it.
It is also strongly heritable, which for decades produced an obvious question and no answer: which genes?
A 2013 study assembled a Swedish national sample of 5,001 cases and 6,243 controls, meta-analysed it with earlier work covering 8,832 cases and 12,067 controls, then tested the leading signals again in 7,413 cases, 19,762 controls and 581 parent-offspring trios.
Twenty-two positions passed genome-wide significance — thirteen of them new. But the finding that mattered most was not any of them individually. It was the estimate the authors derived from the data as a whole:
That is the shape of the thing. Not a gene for schizophrenia; eight thousand positions, each nudging.
The genes near these positions were not a random draw. Several converge on neuronal calcium signalling — most visibly rs1006737 in CACNA1C, which encodes a subunit of a voltage-gated calcium channel.
Calcium entry is how a neuron converts electrical activity into a lasting change, so a set of hits landing there is a biological statement rather than a statistical one. CACNA1C is also one of the clearest points of overlap with bipolar disorder, which is a finding about psychiatric categories as much as about genetics.
These two facts are both true, and the tension between them is where most misreading happens.
Heritability of 32% from common variants means inheritance matters at the level of a population. Eight thousand contributing positions means no individual result is informative: each one moves risk by a fraction of a percent against a lifetime risk of about 1 percent.
Fourteen of those eight thousand are on this page. Reading them tells you nothing about yourself.
Schizophrenia is diagnosed clinically, from symptoms and their course over time. No genotype is used in diagnosis, in predicting onset, or in choosing an antipsychotic. Polygenic scores separate groups and do not classify people.
If this is a live question for you or someone close to you, the thing that changes an outcome is a psychiatric assessment — and early treatment, which is one of the few things in this illness that reliably matters.
Positions joined since this page was written
What this is The text above discusses the variants this page was written around. Since then the catalogue has joined 36 more positions to it, by shared trait or shared paper. They are listed here by the paper each came from; the text does not describe them, and each variant page carries that study's own record.
Autism Spectrum Disorders Working Group of The Psychiatric Genomics Consortium 2017, Molecular autism rs141342723 (GPX5), rs202906 (HIST1H1B), rs707939 (ABHD16A), rs9269271 (HLA-DRA), rs184153866 (HLA-DRB1), rs116182620 (near HLA-DRB5), rs11753207 (HLA-DRB1), rs147976543 (HLA-DRB1), rs72761442 (CTC-436P18.1), rs61789073 (DPYD), rs115443066 (HLA-DQA1) — PMID:28540026
Verma A et al. 2024, Science (New York, N.Y.) rs75381199 (near LINC02379), rs188839242 (ITSN2), rs373182523 (PLCB1), rs115632032 (near UBE3D), rs192439018 (near LINC01673), rs572938512 (LINC02997), rs187751347 (CFAP77) — PMID:39024449
Yao X et al. 2021, Translational psychiatry rs4936216 (near LINC02730), rs6449528 (ZSWIM6), rs10515678 (LINC01470), rs7143919 (RGS6), rs17659437 (near LINC01645), rs439639 (TMTC1), rs10150710 (BCL11B) — PMID:33479212
Tang M et al. 2024, Schizophrenia bulletin rs2905432 (near GATAD2A), rs2532363 (near MAPK8IP1P1), rs7447717 (near HCN1) — PMID:37467357
Li Q et al. 2017, Pharmacogenetics and genomics rs117752187 (MIR100HG), rs76131026 (near KCNIP1) — PMID:27846195
Smith RL et al. 2020, Translational psychiatry rs10023464 (CTD-2005D20.1) — PMID:32555152
Pardiñas AF et al. 2019, The American journal of psychiatry rs11725502 (UGT2B10) — PMID:30922102
Amare AT et al. 2018, JAMA psychiatry rs66486766 (ADAMTSL3) — PMID:29121268
Liao Y et al. 2024, Molecular psychiatry rs3824417 (PTPRD) — PMID:38336841
Chen L et al. 2025, Molecular psychiatry rs117043183 (near WDR11) — PMID:39562719
Wang X et al. 2023, Schizophrenia (Heidelberg, Germany) rs4149181 (SLC22A8) — PMID:37491364
2026-02-13 · Differential genome-wide association analysis of schizophrenia and post-traumatic stress disorder identifies opposing effects at the MAPT/CRHR1 locus. Frontiers in Genetics. 2026. DOI:10.3389/fgene.2026.1728494
The same gene locus pushes schizophrenia risk up and PTSD risk down, in opposite directions
Schizophrenia (SCZ) and post-traumatic stress disorder (PTSD) share some symptoms but are thought to have distinct biology. This study directly compared their genetic architectures using Psychiatric Genomics Consortium summary statistics, finding 4 loci with genome-wide significant differential associations between the two conditions: rs62062288, rs58120505, rs12536395 and rs11057189. All four showed genome-wide significant association with SCZ and nominal association with PTSD, but in opposite directions of effect -- a variant that raises SCZ risk lowers PTSD risk, or vice versa. Only rs62062288, near the MAPT/CRHR1 locus, retained genome-wide significance for this opposing pattern after full correction. MAPT (tau protein, more familiar from Alzheimer's research) and CRHR1 (a stress-hormone receptor gene) both have plausible mechanistic links to stress response and neurodegeneration, making this a genuinely interesting divergence point between two conditions that can otherwise look similar clinically. This site's schizophrenia page carries 175 variants; this locus is a specific, differential addition rather than a general new risk variant.
2025-12-10 · Nature
A study analyzing genetic data from over 1 million cases across 14 psychiatric disorders together, rather than one at a time, found five latent genetic factors explaining about 66% of the genetic variance in the individual disorders, plus 238 loci with effects that cross disorder boundaries. Schizophrenia and bipolar disorder formed one such factor, sharing so much of their genetic signal that the study found very few loci specific to either disorder alone -- that shared factor was linked to gene expression specifically in excitatory neurons. A separate factor grouped major depression, PTSD and anxiety, linked instead to oligodendrocyte biology. The authors frame this as evidence for regrouping psychiatric diagnosis around shared underlying biology rather than the current symptom-based categories. PMID:41372416.
2026-09-11 · Chen Y, Feng Q, Lam M, et al., Nature Genetics
Contribution of copy number variants to schizophrenia in East Asian populations
Rare copy number variant (CNV) studies of schizophrenia had focused almost entirely on European ancestry. This one covers 20,903 East Asian cases and 23,258 controls: cases carried a significantly elevated genome-wide burden of rare CNVs, effects were largely consistent across populations, and nine genome-wide-significant CNV loci were found in the East Asian sample alone. Meta-analysis with European data gave 14 significant loci, 8 of them reaching genome-wide significance for the first time; genes inside them were markedly less tolerant of loss-of-function variants than genes in other CNV loci. The newly found CNVs were far more common in East Asian than European carriers (0.38% vs 0.0017%). CNVs are rare structural variants, not the common single-letter variants this catalogue holds, so this sits alongside the schizophrenia page rather than inside it. PMID:42728386.
The source. Ripke et al. (Nat Genet 2013) conducted a multi-stage GWAS beginning with a Swedish national sample of 5,001 cases and 6,243 controls, meta-analysed with previous schizophrenia GWAS totalling 8,832 cases and 12,067 controls, followed by replication of SNPs in 168 genomic regions in independent samples of 7,413 cases, 19,762 controls and 581 parent-offspring trios. Twenty-two loci reached genome-wide significance, 13 of them new and one previously implicated in bipolar disorder. Earlier signals on this page derive from the 2009 ISC/SGENE reports and subsequent meta-analyses.
Polygenicity. The authors estimated that approximately 8,300 independent, mostly common SNPs (95% credible interval 6,300–10,200) contribute to liability, collectively accounting for at least 32% of variance. This is the quantitative statement that the architecture is extremely polygenic; individual odds ratios at genome-wide significant loci are correspondingly small.
Calcium signalling. Examination of candidate genes at the associated loci implicated neuronal calcium signalling, with CACNA1C (rs1006737) the most-cited example. CACNA1C is among the loci shared with bipolar disorder, and the cross-disorder overlap is itself a replicated finding rather than an artefact of diagnostic imprecision.
MHC. rs13194053 lies in the major histocompatibility complex, the region with the strongest and least tractable schizophrenia signal. Extended linkage disequilibrium across the MHC makes attribution to a gene difficult, and interpretation of any single marker there should be correspondingly cautious.
Clinical use. None of these variants is used diagnostically or prognostically, and none informs antipsychotic selection. Polygenic risk scores for schizophrenia discriminate at the group level and are not clinically actionable for an individual.
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about Schizophrenia comes down to these specific, well-studied positions — not a diagnosis. 212 positions are linked to this page; the ones this page's own text discusses are shown first.
The studies behind these variants recruited participants from different ancestries — a result found in one population doesn't always transfer to another. Based on 188 of 212 linked studies with a resolved discovery ancestry.
Research-derived gene–drug associations only — not a prescription, dosing guide, or medical advice. Always follow your prescriber's guidance.
| Gene | Drug | What the research shows |
|---|---|---|
| CYP2D6 | Aripiprazole and risperidone | Both of these antipsychotics are cleared largely by CYP2D6, and people at the extremes of that enzyme are exposed to markedly different amounts of drug on the same dose. A poor metaboliser accumulates more and is more likely to meet the side effects that make people stop — sedation, restlessness, movement problems — and stopping is the single biggest risk in treating this illness. An ultrarapid metaboliser may not reach a useful level. CPIC rates both pairs level B: the evidence is worth knowing about and has not been turned into a dosing rule, which is what the level means. It says nothing about which antipsychotic will work for a particular person, and nothing here should be used to start, stop or change a medicine. (CPIC lists CYP2D6–aripiprazole and CYP2D6–risperidone at level B; no CPIC guideline has been published for either pair.) |
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Schizophrenia. MyGeneLog™. https://www.mygenelog.com/conditions/schizophrenia
Because the inheritance is spread across roughly 8,300 positions. Heritability is a statement about how variation in a population is distributed; prediction is a statement about one person. With eight thousand contributors each moving risk by a fraction of a percent, the first can be large while the second stays useless.
It encodes a subunit of a voltage-gated calcium channel. Calcium entry is how a neuron turns electrical activity into a lasting change, so hits landing there are a biological claim rather than a statistical coincidence. It is also one of the clearest overlaps between schizophrenia and bipolar disorder.
There is no test to be given. No genotype is used in diagnosis or in predicting onset, and a polygenic score would not change what anybody does. What does matter is knowing that risk in a first-degree relative is elevated, and that early assessment and treatment are among the few things that reliably improve outcomes.
Free to reuse. This page's text is original writing from freely-available research, licensed CC BY 4.0 — reuse it, including commercially, with attribution to MyGeneLog™. It's general research-derived information, not medical advice or a diagnosis — see Terms of Use.