Remarkably the oxidized, secreted form of gal-1 actually promotes axonal regeneration (Horie and Kadoya, 2004) and when administered to ALS mice in recombinant form, it improves motor activity, delays disease onset and prolongs survival of treated animals (Chang-Hong et al., 2005; Kato et al., 2005), highlighting its potential as a therapeutic strategy to stabilize NMJs. This evidence concerns the gene LGALS1 and amyotrophic lateral sclerosis.