The consequences of genetic deletion of C5aR1 reported here support the contention that the mechanism by which the previously used small molecular weight cyclic hexapeptide C5aR1 antagonist, PMX205, was mediating its beneficial effects in AD mouse models [7] was via the inhibition of C5aR1 cell signaling, and support the continued assessment of C5aR1 antagonists for AD therapy. The gene discussed is C5AR1; the disease is Alzheimer disease.