IDO1/2 and TDO overexpression in tumor cells promotes tryptophan depletion in the microenvironment, resulting in suppression of the T-cell mediated immune response. IDO1/2 and TDO catalyze the breakdown of tryptophan into kynurenine, and KMO plays a key role in that pathway, hydroxylating kynurenine into 3-hydroxykynurenine. KMO is required for the synthesis of quinolinic acid, a neurotoxic NMDA receptor antagonist involved in axonal targeting, synaptogenesis and apoptosis during brain development. KMO activity has been linked to Huntington’s (HD) and Alzheimer’s diseases, and research shows that KMO inhibitors can improve the lifespan of Huntington's disease mice. In addition to being a therapeutic target for neurological disorders, elevated KMO also is an indicator of renal and hepatocellular carcinoma, suggesting KMO may have value as a prognostic biomarker.