Recently, in a Drosophila model of ALS based on TAR DNA-binding protein 43 (TDP-43) that recapitulates several aspects of ALS pathophysiology, pioglitazone rescued TDP-43-dependent locomotor dysfunction in motoneurons and glia but not in muscles and also was neuroprotective when FUS, but not SOD1, is expressed in motoneurons [81]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.