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). The gene discussed is KDM1A; the disease is amyotrophic lateral sclerosis.