Genetic studies conducted in the roundworm Caenorhabditis elegans revealed that combined suppression of ufd-2 and spr-5, whose human orthologs are UBE4B and KDM1A, respectively, resulted in robust suppression of neurotoxicity driven by the amyotrophic lateral sclerosis (ALS)–linked SOD1G85R mutation (181). This evidence concerns the gene UBE4B and amyotrophic lateral sclerosis.