In contrast, in a Drosophila model carrying ALS-FUS mutations, depletion of endogenous arginine methyltransferase 1 (DART1), which is orthologous to human PRMT1 and PRMT8, enhanced the neurodegenerative phenotype introduced by FUS overexpression in fly eyes [78]. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.