Xiaoyang Shan et al. discovered reduced protein O-glycosylation in the nervous system of the mutant SOD1 transgenic mouse model of ALS, with decreased O-GlcNAc immunoreactivity levels in spinal cord tissue from mSOD mice compared to controls, indicating that the neurodegeneration observed in mSOD mice is linked to a decrease in O-GlcNAc levels in neurons, including motor neurons [92]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.