Astrocytes derived from ALS-hiPSCs carrying mutations in VCP, SOD1 and C9ORF72 genes exhibit aberrant intron retention [206]; intron retention is a mechanism to suppress translation, and thus, the increased translation of a number of reactivity genes was observed in the mutant astrocytes, likely contributing to their entrance into a reactive state [206]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.