But microglial-specific Ifnar1 deletion only ameliorates post-synaptic loss, while neural-specific Ifnar1 deletion not only improves pre-synaptic loss but also decreases Aβ plaque burden, meaning that IFN-I inhibition attenuates AD pathologies by preventing microglia-mediated inflammation and its phagocytosis to postsynaptic structure, as well as neuron-mediated Aβ release from pre-synaptic membrane (Roy et al, 2022). The gene discussed is IFNAR1; the disease is Alzheimer disease.