In conclusion, we propose the following as potential therapeutic targets for regulation in SOD1-ALS: (1) transcription factors that induce microglia into proinflammatory phenotypes, such as Irf8 or C/EBPs, (2) molecules involved in the TREM2-APOE pathway, especially TREM2, and (3) astrocyte function involved in the dysregulation of lipids. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.