Increased levels of ROS and ROS-induced damage to DNA, RNA, proteins and lipids [111], and perturbations of calcium homeostasis have been observed in in vitro and in vivo ALS models harbouring mutations in SOD1, TDP-43, and FUS/TLS and in the motor nerve terminals of ALS patients [112,113,114,115,116,117,118]. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.