In addition, comparison analysis between the respective FUS-ALS and SOD1-ALS DEGs across different datasets (present study vs. GSE106382) was also performed because we wanted to focus on common regulatory mechanisms and/or molecular footprints at the pathway level and to better understand the link and the differences encompassed in the development of the two manifestations of these diseases. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.