GLT1 is the analog to EAAT2 in rodent astroglial cells, however, hypermethylation on specific CpG islands of GLT1 promoter was discovered to participate in repression of GLT1 promoter activation, whereas this regulation was not involved in astroglial dysfunction of EAAT2 in ALS patients (Yang et al., 2010). This evidence concerns the gene SLC1A2 and amyotrophic lateral sclerosis.