Since the intraneuronal deposits of hyperphosphorylated tau proteins constitute one of the two main features of Alzheimer’s disease in combination with Aβ, the apparent induction of tau and Aβ phagocytosis by CX3CR1 activation could be a protective mechanism as relevant as the well-known limitation of microglial activation. Here, CX3CR1 is linked to early-onset autosomal dominant Alzheimer disease.