In the January 1999 issue of the ARCHIVES, Farber et al1 commented on 2 recent clinical trials of glycinergic agents used to treat schizophrenia. The commentary, overall, supported the concept that underactivity of N-methyl-D-aspartate (NMDA) receptor–mediated neurotransmission may play a crucial role in the pathophysiology of schizophrenia. However, we feel it is important to discuss 3 specific issues raised in that commentary.