Therefore, even if the pathophysiology of DM mimics only a fraction of ALS cases (namely, those mediated by SOD1 mutations), DM may remain a useful animal model for ALS insofar as it could afford us insights into the interplay between the unfolded protein response (UPR) of microglia and astrocytes and the spinal cord inflammation seen in the two diseases. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.