Recent studies have shown astrocyte dysfunction in HD [15] and mHTT led to the loss of neuron protection against N-methyl-D-aspartate (NMDA) toxicity, reduced capacity to buffer extracellular K+ [16], impaired glutamate transport, dysfunction in proinflammatory mediators and anti-inflammatory cytokines, astrocytic mitochondrial dysfunction, compromised the release of trophic factors brain-derived neurotrophic factor (BDNF) and chemokine Ccl5/RANTES [13]. The gene discussed is CCL5; the disease is Huntington disease.