To establish whether loss of functional EAAT2 in ALS was a primary cause of neuron degeneration or a consequence of cell damage, transgenic mutant SOD1 mice overexpressing EAAT2 (EAAT2/G93A double transgenic mice) were generated to investigate whether supplementation of EAAT2 loss would delay or rescue the disease. Here, SLC1A2 is linked to amyotrophic lateral sclerosis.