Several studies have confirmed these intricate aspects of ALS pathogenesis using different animal models, including SOD1 transgenic mice [48,53], FUS mutant mice, or Drosophila [49,50,51,52], as well as mice with TDP-43 deletion [58] or overexpression [54,55,56,57]. This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.