Having confirmed the selectivity of αCCR2 and ruled out its non-specific effect on cognition, we next tested in DM-hTAU mice, an animal model of tauopathy, whether blocking of CCR2 would abrogate the beneficial response of αPD-L1 treatment, and if so, which additional cells beyond the monocytes are involved in such a therapeutic effect. The gene discussed is CCR2; the disease is tauopathy.