It is important to note that in sporadic amyotrophic lateral sclerosis (ALS) patients, multiple abnormal glutamate transporter EAAT2 (GLT-1) variant splicing with intron retention or exon skipping has been shown to result in the loss of EAAT2 protein activity but contributes to pathogenesis of the disease [32]. This evidence concerns the gene SLC1A2 and sporadic amyotrophic lateral sclerosis.