Decreased EAAT1 and EAAT2 levels suggest that C9-HRE astrocytes may not be able to efficiently take up excessive glutamate from synaptic cleft, which might lead to glutamate excitotoxicity, especially as induced motor neurons of C9-HRE ALS patients and C9orf72-deficient motor neurons have higher levels of glutamate receptors in neurites and dendritic spines (Shi et al., 2018). Here, C9 is linked to amyotrophic lateral sclerosis.