Previous studies in our lab, and others, have shown that the genetic or pharmacological inhibition of C5a‐C5aR1 signaling reduced pathology, and rescued synaptic and cognitive loss in several mouse models of AD,29, 30, 31, 32, 33 suggesting that C5a‐C5aR1 signaling might be a better therapeutic target than blocking the upstream components of the complement cascade. The gene discussed is C5; the disease is Alzheimer disease.