Additionally, ADSC-Exo could decrease the aggregation of mutant superoxide dismutase 1 (SOD-1) in G93A neurons, reduce abnormally expressed mitochondrial functional proteins, and restore the normal cell phenotype of amyotrophic lateral sclerosis (ALS), suggesting a therapeutic potential of ADSC-Exo in ALS [54]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.