The presence of reactive astrogliosis, the activation of microglial cells, and the up-regulation of the proinflammatory cytokines TNF-α and IL-1β in the cerebella of the iPLA2β-/- mice suggest that inflammation occurs and inflammation-mediated neurotoxicity may play a role in the pathogenesis of cerebellar atrophy in INAD. The gene discussed is TNF; the disease is neurodegeneration with brain iron accumulation 2A.