When primary astrocytes are cultured in media containing mitochondria released from microglia activated in a model of Huntington’s disease (HD) or lipopoly-saccharide (LPS)-induced neuroinflammation, their phenotype switches to the proinflammatory A1 type, with a several-fold increase in proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β), as well as exhibiting mitochondrial rupture, dysfunction, and exacerbated cell death [117]. The gene discussed is TNF; the disease is juvenile Huntington disease.