Glutamatergic hypothesis has gained increasing support explaining symptoms of schizophrenia, and hypofunction of N-methyl-D-aspartate (NMDA) receptor is considered nowadays a major factor in the pathophysiology of the disease. Several NMDA-enhancing agents such as glycine, D-alanine, D-serine, sarcosine and bitopertin have shown beneficial effect as add-on treatments to antipsychotics. D-amino acid oxidase (DAAO) metabolizes D-alanine and D-serine, which are co-agonists of NMDA-receptor, and, therefore, decreasing DAAO activity results into enhancement of NMDA-receptor function. Recently, a randomized controlled trial in 52 patients with chronic schizophrenia was well tolerated and showed a robust beneficial effect of DAAO inhibitor sodium benzoate (1 g/d) as compared with placebo (effect size 1.76 for PANSS total scores; Tsai et al. 2012).