In addition, there is cross-talk between astrocytes and microglia via IL-3, which promotes microglia-based attenuation of Aβ pathology in AD [106], raising the possibility that the protective action of the N-terminal Aβ fragments may also involve downstream regulation of astrocyte–microglia interactions, which will be considered in future studies, as well. The gene discussed is IL3; the disease is Alzheimer disease.