This finding not only indicates that the metabolic imbalance of the kynurenine metabolic pathway (the accumulation of toxic products and depletion of protective substances) is a key pathological bridge to reducing the risk of cognitive inhibition in epilepsy-depression co-morbidities, but also suggests that the KMO could be a “dual-action” target, which could be the basis for the development of innovative therapies with both antiepileptic and anti-depressant effects. This evidence concerns the gene KMO and major depressive disorder.