Previous research has also shown that pro-inflammatory cytokines released by activated microglia near amyloid plaques, including TNFα, IFNγ, and IL-1β, can increase Aβ peptide levels and decrease amyloid plaque clearance [63–66], promoting a positive feedback cycle between amyloid plaque deposition, microglial activation, neutrophil/immune cell recruitment, and neuroinflammation, which may further support our findings. The gene discussed is IL1B; the disease is amyloidosis.