According to the results of other study focusing on cultured primary brain cells from G93A mice carrying ALS phenotype, EVs from ADSC were capable to reduce level of harmful SOD1 aggregates in such neural cells and upregulate levels of phosphorylated cAMP response element-binding protein (p-CREB) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)—the mitochondrial proteins, which are decreased during ALS development and progression [47]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.