In many animal models (ALS SOD1G93A mouse and rat models, as well as TDP43 ALS mouse models) and patients with ALS, a significant reduction in the expression of the EAAT2 gene in reactive astrocytes has been observed, leading to an accumulation of excess glutamate in the extracellular synaptic cleft. This evidence concerns the gene SLC1A2 and amyotrophic lateral sclerosis.