Current treatment of schizophrenia offers a wide variety of psychopharmaceuticals that are licensed as first-line treatments for this disorder. However, if we consider their dominant mechanism of action, choice eventually narrows, in some instances considerably. In light of the facts that one third of patients do not respond to standard treatment and that current treatment options do not affect all schizophrenia symptom dimensions, it is not hard to conclude that there is an unsatisfied need which should drive the development of new treatment modalities focusing on other neurotransmitter systems beside dopamine and serotonin [1]. There have been recent discoveries in terms of convergent and convincing evidence from pharmacological, autoimmune, and genetic studies which have confirmed that impaired glutamatergic N-methyl-D-aspartate (NMDA) receptor function can produce psychotic symptoms and that it is involved in the pathogenesis of schizophrenia. Glycine transporters 1 (GlyT1) play a key role in terminating the activity of glycine, which is released into synapses from glial cells to bind