In contrast, in Gabrb2 knockout, the absence of the GABAA-receptor β2 subunit was clearly the root of the schizophrenia-like phenotypes and comorbidities of the KO mice, with no major divergence from the positive symptoms, negative symptoms and cognitive deficit of schizophrenia, and reversible in part or in full by risperidone for a number of the symptoms. This evidence concerns the gene GABRB2 and schizophrenia.