To further investigate the role of Miro1 in the axonal transport defects observed in ALS mutant SOD1-expressing neurons we enquired if expressing wild type Miro1 or a Ca2+ insensitive mutant of Miro1 in which the EF hands were disrupted (Miro1E208K/E328K) could rescue the effect of ALS mutant SOD1 on mitochondrial transport. The gene discussed is RHOT1; the disease is amyotrophic lateral sclerosis.