More specific to astrocytes, the effects of an increased LPS/HMGB1-TLR4/YY1 pathway results in the YY1 suppression of EAAT2 in astrocytes [165], leading to upregulated glutamatergic activity and associated excitotoxicity in MNs, which is the rationale for the use of Riluzole in ALS treatment. The gene discussed is YY1; the disease is amyotrophic lateral sclerosis.