In a cellular ALS model, it has been shown that SOD1G93A inhibits the glycosylation of GPNMB, resulting in increased motoneuron death (33) and treatment with recombinant extracellular fragments of GPNMB (rGPNMB) leads to diminished cell death (33, 34). This evidence concerns the gene GPNMB and amyotrophic lateral sclerosis.