Mutations across TDP-43, FUS, and SOD1 have also long been known to trigger stress response pathways that ensue in global miRNA reductions [67], with associated deregulated pathways confirming multiple disease-related mechanisms including synaptic vesicle and cell cycle dysregulation before downstream MN degeneration, but these mechanisms fail to confer ALS specificity, or at least effectiveness in therapy [163]. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.