To investigate the biological significance of the interaction of FUS with PRMT1 and PRMT8, we used a Drosophila model of FUS-related ALS that we recently developed and that recapitulates several key features of human ALS, such as mutation-dependent toxicity, mislocalization of mutant FUS into the cytoplasm, and behavioral defects [20]. The gene discussed is PRMT8; the disease is amyotrophic lateral sclerosis.