Besides the beneficial role of genetic ablation of C5aR1 in preventing the loss of neurite complexity, presynaptic loss (data reported in this manuscript) and cognitive deficits in the Arctic mouse model of AD,29, 33 pharmacological inhibition of C5a‐C5aR1 signaling with PMX205, a potent C5aR1 antagonist,31, 32 in two different mouse models of AD has shown beneficial effects in modulating gene expression and preventing synaptic and cognitive deficits. The gene discussed is C5; the disease is Cognitive impairment.