Since the publication of the most recent GRM3 meta-analysis, 12 there have been three additional studies published involving 6027 (2381 schizophrenia and 3646 control) individuals, 2, 6, 13 indicating a reappraisal is warranted. Furthermore, neither of the previous meta-analyses included family-based genetic association studies, which may have biased their results. This is in contrast to the PGC genome-wide association study (GWAS) that predominately included individuals of European descent, suggesting that the association between GRM3 and schizophrenia may be population specific. Importantly, in both these meta-analyses, the included studies primarily comprised individuals from Asian populations. 5 However, two meta-analyses of GRM3 SNPs have failed to support an association with schizophrenia risk. 1 This PGC finding complements a number of previous associations between GRM3 and schizophrenia-related phenotypes, such as prefrontal activation during cognitive tasks, 2 white matter integrity, 3 hippocampal volume in severe obstetric complications, 4 poor cognitive performance (that is, verbal fluency, digit symbol test, perseverative error processing and spatial working memory), 5, 6, 7, 8, 9 antipsychotic response in first-episode schizophrenia 10 and positive symptoms severity in treatment-resistant schizophrenia. 1 Among these associations, the metabotropic glutamate receptor 3 ( GRM3) contained the second most significant single-nucleotide polymorphism (SNP) (rs12704290, P=3.33 × 10 −10). The Schizophrenia Working Group of the Psychiatric Genomics Consortium (PGC) has identified several significant genome-wide associations between genes involved in glutamatergic neurotransmission and schizophrenia. Our findings support the GWAS-implicated link between GRM3 genetic variation and schizophrenia risk as well as the notion that alleles conferring this risk may be population specific. We also found evidence for population stratification related to rs2237562 in that the ‘risk’ allele was dependent on the population under study. Two of these SNPs (rs2237562, rs917071) were in strong-to-moderate linkage disequilibrium with the top GRM3 GWAS significant SNP (rs12704290) reported by the Schizophrenia Working Group of the Psychiatric Genomics Consortium. To reconcile these conflicting findings, we conducted the largest and most comprehensive meta-analysis of 14 SNPs in GRM3 from a total of 11 318 schizophrenia cases, 13 820 controls and 486 parent–proband trios. However, previous meta-analyses have refuted the association between GRM3 single-nucleotide polymorphisms (SNPs) and schizophrenia risk. Genome-wide association study (GWAS) evidence has identified the metabotropic glutamate receptor 3 ( GRM3) gene as a potential harbor for schizophrenia risk variants.