In a FUSR521C mouse model of ALS, overexpression of PRMT1 rescues neurite growth associated with oxidative stress [164] through a mechanism that involves PRMT1 interacting with FUS leading to a stable complex of FUS/PRMT1/Nd1-L causing inhibition of PRMT1 activity. The gene discussed is PRMT1; the disease is amyotrophic lateral sclerosis.