SOD1 and amyotrophic lateral sclerosis: Similar results were reproduced when analyzing human iPSC astrocytes derived from mutant SOD1 and C9orf72 ALS patients, as well as from astrocytes stimulated with TNFα, IL-1β, and C1q, indicating that diminished intron retention is a general feature of reactive astrocytes, including those generated by ALS pathogenic mutant genes.