The overexpression of EAAT2 (Guo et al. 2003) and the pharmacologically induced up-regulation of EAAT2 transcription could show beneficial effects in ALS model mice (Rothstein et al. 2005); suggesting that decreased EAAT2 expression is rather a cause than a consequence of ALS. This evidence concerns the gene SLC1A2 and amyotrophic lateral sclerosis.