Schizophrenia is a relatively common but genetically complex disorder, making the identification of susceptibility genes formidable. However, progress in genetic studies on schizophrenia during the past ten years has revealed several replicated linkage loci, which span over multiple chromosomal regions. Since last year, several causal genes have been isolated from those linkage regions. All of these have proven to have some functional relevance to glutamatergic neurotransmission. These results are interesting because the "hypoglutamatergic hypothesis" for pathophysiology of schizophrenia has been articulated since the early eighties. This hypothesis has been supported both by pharmacological evidence that administration of NMDA-type glutamate receptor antagonists induces schizophrenia-like symptoms and by neurophysiological studies. Recent lines of evidence from a candidate gene approach have also endorsed the hypothesis. Here, we introduce the overview of recent progress in genetic studies that converge to depict the hypothesis of glutamatergic hypofunction in schizophrenia.