Regarding the glutamate transporter dysfunction, decreased high-affinity glutamate transport [194], a decrease in expression levels of EAAT2 [195], the expression of abnormal intron 7-including EAAT2 mRNA [196], and an increase of EAAT2 pre-mRNA with RNA edited intron 7 [197] have been reported in ALS patients (Figure 2). The gene discussed is SLC1A2; the disease is amyotrophic lateral sclerosis.