For instance, Devoy and colleagues created a mouse model of ALS harboring a human-associated frameshift mutation in FUS (p.G466VfsX14), and found progressive motor neuron degeneration in 15-month-old mice without aggregation of aberrant proteins (Devoy et al., 2017), which could be explained by the functional redundancy between FUS and other FET proteins that occurs in neurons (Kabashi et al., 2011; Sasayama et al., 2012). The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.