This raises an intriguing possibility that SCA31 repeat RNAs and ALS-causing factors such as TDP43, FUS, and HNRNPA2B1 could interact to neutralize the respective toxic effects, suggesting that the disruption induced by aberrant expansion of the SCA31 repeat and the TDP43 mutation could be responsible for the neurodegenerative disease phenotypes [39]. The gene discussed is BEAN1; the disease is amyotrophic lateral sclerosis.