C9orf72 and amyotrophic lateral sclerosis: In both C9ORF72-ALS human-derived neurons and G4C2x36 Drosophila, the expression of approximately one third of the SRSF1-RNAi-manipulated transcripts altered in disease is completely reversed upon neuroprotective depletion of SRSF1, revealing in turn in vitro and in vivo C9ORF72-ALS disease-modifying small gene expression signatures.