Kato, Y., and Sakamoto, K. (2021), in a cell model of amyotrophic lateral sclerosis (ALS), showed that this drug attenuates morphological changes under stress, activates mitophagy via the PINK1-Parkin-ubiquitin pathway, prevents transactive response DNA binding protein 43 kDa (TDP-43) mislocalization, and promotes degradation of TDP-43 aggregates, and therefore may be a candidate drug for ALS treatment [75]. This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.