Previous studies showed that overexpression of Nogo-A in skeletal muscle was associated with NMJ dysfunction in ALS patients, and that inhibition of Nogo-A–NgR1 binding by anti–Nogo-A antibodies improved distal axonal degeneration and NMJ function and slowed disease progression in ALS model mice [11–13, 16]. The gene discussed is RTN4R; the disease is amyotrophic lateral sclerosis.