While our previous studies have shown that a deletion of Cx3cr1 in B6 mice augments microglial uptake of exogenously injected Aβ42 [25], the role of CX3CR1 in microglial phagocytosis of endogenously produced, extracellular fAβ plaques in the context of accumulating AD pathology is largely unclear. The gene discussed is FANCB; the disease is Alzheimer disease.