SOD1 and amyotrophic lateral sclerosis: Our results suggest that chronically accelerated turnover of mitochondrial OMM proteins involved in mitochondrial dynamics and transport leads to their depletion resulting in the defects of mitochondria fusion and transport, which are well characterized in mutant SOD1 animal and cellular models and in other forms of ALS, such as TDP‐43 mutants (Magrane & Manfredi, 2009; Smith et al, 2017).