Combined with cumulative evidence of a reciprocal interaction between glutamatergic/NMDAR hypofunction and oxidative stress impacting on parvalbumin interneurons and cognition in schizophrenia [67–69], our finding of EAAT3 abnormalities as well as its association with cognition in RESP but disrupted in TRS + LRS group may provide a novel molecular target for improving cognition in individuals with treatment resistance. The gene discussed is SLC1A1; the disease is schizophrenia.