In particular, among the most recently described mutations in the ALS–FTD spectrum of neurodegeneration, TBK1 loss-of-function mutations, producing premature termination codons that cause nonsense-mediated mRNA decay and resulting in the loss of mutant transcript and subsequent loss or reduction of TBK1 protein, has been associated with both ALS and FTD [58,59]. This evidence concerns the gene TBK1 and amyotrophic lateral sclerosis.