This most likely culminates from protein misfolding and insolubility resulting in neurodegeneration, analogous to what is seen in Alzheimer’s and Parkinson’s diseases, where such aggregation only further implies the prion-like properties of TDP-43, FUS, and possibly all known RBPs in the context of ALS and NDs [13,148]. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.