These data are consistent with our previous results, showing an increase of S100A4 in the microglia and astrocytes from a SOD1 rat model in vivo and in mutant SOD1 fibroblasts in vitro [59] and suggest that an increased level of S100A4 is a common pathological trait of ALS, shared by different experimental models and disease-associated gene variants. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.