In the case of AD, targets such as Aβ or NFTs are recognized by TLRs resulting in a proinflammatory cytokine storm associated with release of TNF, IL-1 and NO, while recognition of cell debris or dystrophic neurites by microglial TREM2 receptors is associated with a phagocytic response along with an increase in TGFB and IL10 signaling (Neumann and Takahashi, 2007; Takahashi et al., 2007; Neumann et al., 2009). The gene discussed is TGFB1; the disease is Alzheimer disease.