Using transgenic mouse models of AD, with the overexpression of microglial RAGE and the amyloid precursor protein (APP), Fang et al. showed that amyloid β was in part responsible for the increased production of the pro-inflammatory cytokines IL-1β and TNF-α by the microglia in a RAGE-dependent manner (Figure 5) [78]. This evidence concerns the gene IL1B and Alzheimer disease.