After revealing the multilevel misregulation of Parkin and PINK1 by TDP-43 OE at the cellular level, we were keen to know whether their misregulations contribute to ALS pathogenesis and whether restoring Parkin and PINK1 normal expression levels offers a means to ameliorate TDP-43-mediated neurodegeneration at the animal level. Here, PRKN is linked to amyotrophic lateral sclerosis.