Our previous in vivo investigations in the adult G127X SOD1 mouse model of ALS have confirmed a presymptomatic increase in Na+ current in distal peripheral motor axons27 and a disruption of axonal potassium channels related to a breakdown of nodal organisation in the ventral roots of these mice, assumed to be indicative of axonal degeneration28. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.