KYAT1 catalyzes the transamination of L-kynurenine to kynurenic acid, a key intermediate in tryptophan catabolism that acts as a broad-spectrum antagonist of ionotropic glutamate receptors. The enzyme also processes cysteine and selenocysteine conjugates of halogenated compounds through beta-elimination reactions. KYAT1 is expressed in both cytosolic and mitochondrial compartments and functions as a homodimer. In the central nervous system, KYAT1 expression is elevated in the anterior cingulate cortex of individuals with major depressive disorder, suggesting involvement in glutamatergic dysfunction through increased production of the NMDA receptor antagonist kynurenic acid. Plasma KYAT1 levels distinguish patients with schizophrenia from healthy controls and show restoration toward normal levels following paliperidone palmitate maintenance therapy, positioning it as a treatment-responsive biomarker 1. Expression of KYAT1 mRNA is increased in depression, indicating enhanced activation of the kynurenic acid arm of the kynurenine pathway 2. In oncology, KYAT1 has emerged as a therapeutic target in hepatocellular carcinoma. Tumor-specific induction of KYAT1 combined with selenocysteine metabolite treatment enhanced cytotoxicity through reactive oxygen species formation, with selectivity for cancer cells achieved through microRNA-guided regulation 3. KYAT1 expression in head and neck squamous cell carcinomas is upregulated by conventional chemotherapy and immunotherapy but suppressed by the CDK inhibitor dinaciclib, highlighting therapeutic resistance mechanisms 4. KYAT1 also appears as a circulating biomarker associated with hepatic steatosis in Prader-Willi syndrome 5 and COVID-19 severity 6.