Previous work by Chakrabarty et al. has shown that decreased neuroinflammation, brought on by anti-inflammatory cytokines, such as Interleukin-10 or Interleukin-4, suppresses microglial phagocytosis of Aβ plaques and worsens cognitive deficits in APP mice [72, 73], whereas upregulation of the proinflammatory cytokines, Interleukin-6, Interferon γ or Tumor Necrosis Factor α, results in a reduction of Aβ plaque deposition [52, 74, 75]. The gene discussed is IL4; the disease is Cognitive impairment.