Moreover, considering that KP dysregulation contributes to Alzheimer’s disease and amyotrophic lateral sclerosis, where excessive QUIN, reduced KYNA, and redox imbalance are common [7,27,40], FAB’s capacity to restore KYNA production and blunt QUIN-driven excitotoxicity positions it as a promising candidate for chronic inflammatory and neurodegenerative conditions. The gene discussed is NPPA; the disease is early-onset autosomal dominant Alzheimer disease.