Although it is possible that glial populations in mouse models of HD may not fully recapitulate changes to gene expression that are observed in human glial populations in HD, our gene expression data suggest that IL-6 deficiency does not alter innate immune activation in an HD context, but rather may aggravate HD model phenotypes in part by dysregulation of genes related to synaptic transmission and neurotrophin signaling, two pathways that have been linked to mHTT pathogenesis [25, 26]. Here, BDNF is linked to Huntington disease.