Although they reported decreased plaque burden and reduced levels of insoluble Aβ in an AD mouse model after CD14 deletion, loss of this TLR2/4 coreceptor expression was associated with increased expression of genes encoding the pro-inflammatory cytokines TNF-α and Ifnγ, decreased levels of the microglial/macrophage alternative activation markers Fizz1 and Ym1, and increased expression of the anti-inflammatory gene IL-10 [17]. Here, TNF is linked to Alzheimer disease.