In our recent study, in addition to elucidating the pathogenic mechanism of FUS-associated ALS in both Drosophila and animal systems, we found that overexpression of GstO2, a Drosophila homolog of human GSTO1, reduces cytoplasmic FUS aggregates and attenuates neurodegenerative phenotypes, including mitochondrial dysfunction and neuronal toxicity148. This evidence concerns the gene GSTO1 and amyotrophic lateral sclerosis.