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]. The gene discussed is PRMT1; the disease is amyotrophic lateral sclerosis.