Further support for the synaptic dysfunction hypothesis of schizophrenia is suggested by the alteration of genes related to GABAergic and glutamatergic function, including GABAergic gene GAD1 (also known as GAD67; Figure 2), GABAA receptor subunits alpha 5 and delta (GABRA5 and GABRD), and ionotropic NMDA type glutamate receptor subunit NR3B (GRIN3B). The gene discussed is GABRD; the disease is schizophrenia.