Given that the loss of EAAT2 protein and function significantly contributes to excitotoxicity in ALS 8, and that EAAT2 is responsible for clearing approximately 90% of glutamate from the synaptic cleft and plays a key role in regulating excitotoxicity and neuronal death 69, 70, we further examined EAAT2 expression in the motor cortex of C9orf72-ALS/FTD patients. This evidence concerns the gene SLC1A2 and amyotrophic lateral sclerosis.