Thus, in agreement with a PINK1/Parkin-dependent reduction in Miro1 levels as the underlying cause of the ALS mutant SOD1-associated defect in mitochondrial trafficking, miRNA-mediated knockdown of PINK1 rescued mitochondrial axonal transport in SOD1 G93A-expressing cortical and motor neurons. The gene discussed is PINK1; the disease is amyotrophic lateral sclerosis.