In agreement with mitochondrial damage-associated reductions in Miro1 causing axonal transport defects in non-SOD1 ALS, decreased levels of Miro1 have been reported in TDP-43 M337V transgenic mice and in ALS patients (31), and, in the case of FUS, a genetic interaction with PINK1/Parkin has been described in Drosophila (52). Here, SOD1 is linked to amyotrophic lateral sclerosis.