Particularly, in SOD1 mutant MNs we found that cell growth/differentiation and p53-signaling were the most enriched pathways for the miR-10b-5p target genes, which is in line with several studies demonstrating significant involvement of p53 and related cyclin-dependent kinases (CDKs) in various cell responses to stresses, such as DNA damage, hypoxia and MN cell death both in spinal MNs of ALS patients and in ALS mouse models (Dash et al., 2024; Ranganathan and Bowser, 2010). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.