Alternatively, a decrease in levels of NMDAR co-agonists (D-serine, glycine; for example due to genetic changes in the schizophrenia risk genes SR, DAO, or DAOA/G72) or increased levels of endogenous NMDAR blockers such as zinc or kynurenic acid, could play a role (Figure 1). The gene discussed is DAO; the disease is schizophrenia.