The main proposed interrupted mechanisms by most genes mutated in ALS include disrupted proteostasis by increased protein aggregation (SOD1, TARDBP, FUS, C9orf72) decreased proteasomal degradation (VCP, UBQLN2), or impaired autophagy (OPTN, TBK1, CYLD, C9orf72, ALS2, SQSTM1, VCP, UBQLN2, CHMP2B). This evidence concerns the gene CYLD and amyotrophic lateral sclerosis.