Because dephosphorylation of Drp1 was found to be one of the events associated with enhanced mitochondrial fission and neurodegeneration in the ALS models, we explored the upstream phosphatase(s) responsible for this dephosphorylation, under the assumption that upstream phosphatase activation may cause the Drp1-dependent mitochondrial defects found in ALS models (Fig. 3). Here, DNM1L is linked to amyotrophic lateral sclerosis.