To bridge these gaps, future work should (1) quantify KMO activity and downstream metabolites directly in ocular fluids or post-mortem retina, (2) expand and diversify patient cohorts with rigorous adjustment for multiple comparisons, (3) employ longitudinal designs linking baseline KMO levels to rates of visual field loss and RNFL thinning, and (4) evaluate KMO inhibitors—alone and in combination with NMDA antagonists (e.g., memantine) and antioxidants (e.g., N-acetylcysteine)—in glaucoma-relevant animal models. Here, KMO is linked to glaucoma.