The selective removal of mutant SOD1 from NG2+ oligodendrocyte progenitors, but not mature oligodendrocytes in SOD1G37R mice, leads to delayed disease onset and prolonged survival (Kang et al., 2013), further suggesting that mutant SOD1-induced oligodendrocyte defects are detrimental to MNs in ALS. Here, SOD1 is linked to amyotrophic lateral sclerosis.