The overexpression of S100A4 on activated glial cells found in ALS rodent models, together with the increase of vimentin and α-smooth muscular actin in the affected regions, suggested that in addition to its well-known functions in regulating inflammation and cell motility, S100A4 participates in the induction of reactive gliosis and in the formation of the so-called “glial scar” [61]. This evidence concerns the gene S100A4 and amyotrophic lateral sclerosis.