Whether mitochondrial axonal transport defects are part of all ALS is not yet clear, but mitochondrial damage (Sasaki and Iwata, 2007, Allen et al., 2015), dysfunctional calcium metabolism (Curti et al., 1996, Siklos et al., 1996) and reduced expression of Miro1 (Zhang et al., 2015) have been found in sporadic ALS cases. This evidence concerns the gene RHOT1 and amyotrophic lateral sclerosis.