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Lack of glutathione which is one of the important antioxidant and neuroprotective agents in the brain is shown in schizophrenia. This deficiency may be involved in the pathophysiology of the disease as it has been reported. While glutathione can not pass the blood brain barrier (BBB) due to its moleculer structure, N-acetylcysteine (NAC) which is a precursor of glutathione can pass BBB and transform to glutathione and shows neuroprotective and antioxidant effects. In addition, glutathione regulates binding of glutamate to NMDA receptors. In literature, addition of NAC to current treatment, has been reported to provide improvement in symptoms in patients with schizophrenia. The contribution of the use of NAC treatment in a treatment resistant patient with diagnosis of schizoaffective disorder followed in our clinic is presented here. OG is 42-year-old male, married, retired police officer because of disability, a patient with a diagnosis of schizoaffective disorder for 15 years. The patient has been followed up in different clinics on various antipsychotics (paliperidone, aripiprazole, haloperidol, olanzapine, amisulpride, sertindole) and mood stabilizers (lithium, valproic acid). Three years ago, a progressive dose increase in clozapine treatment was decided due to tardive dyskinesia and lack of remission; lithium and other antipsychiotics (olanzapine and amisulpride)were stopped; valproic acid andlamotrigine was added as a mood stabilizer. Symptoms of tardive dyskinesia were decreased in order to control the patient’s delusions. There was a decline in the patient’s complaints upon titration of dose of clozapine to 600mg/day and he largely entered remission for about a year. However the patient’s tardive dyskinesia symptoms emerged again within the last one year; in addition tremor increased, development of a torsioned posture tilted the whole body to the right side (Pisa syndrome). Then patient’s clozapine dose was reduced. Positive and Negative Syndrome Scale (PANNS) and Clinical Global Impression-Severity Scale (CGIS) scores were 84 and 7, respectively. To assess the patient’s tardive dyskinesia, Rockland Simpson Tardive Dyskinesia Rating Scale (RSTDRS) was applied; The scores were as follows: head shaking:5, finger counting:5, restless legs:5, akathisia:5, torsion movements of the body:4 points. His psychotic symptoms were thought to be resistant to treatment so NAC 1200mg/day was added. Four weeks later, patient’s symptoms reduced noticeably. No side effect has been detected during the next 4 months while patient has taken NAC regularly. The patient’s current treatment is clozapine 300 mg/day, lamotrigine 100 mg/day, valproic acid 750 mg/day, NAC 1200mg/day and PANNS, Young Mania Rating Scale, CGIS scores were 50, 7 and 4, respectively. With reduction of symptoms of tardive dyskinesia in patients with the use of NAC, RSTDRS scores were recorded as şoolws: head shaking:2, finger counting:2, restless legs:1, akathisia:0, torsion movements of the body:0 points. Patient’s auditory hallucinations, persecutive and grandiose delusions have regressed. NAC supplementation may have positive impact on the treatment resistant schizophrenia as it has been reported previously. In this case, notwithstanding reduction in psychotic symptoms, negative symptoms were still observed. Perhaps, this could be due to short duration of NAC treatment. NAC has a much tolerable side effect profile than currently used antipsychotic drugs and can be safely combined with other drugs. For all these reasons, NAC may be considered in the forefront as an option for early prevention of psychotic symptoms and tardive dyskinesia.