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). The gene discussed is OPTN; the disease is amyotrophic lateral sclerosis.