The upregulated profiles of complement proteins in AD brain [61–63] and the demonstrated safety of the suppression of C5a generation or C5aR1 signaling in human patients with inflammatory diseases [64, 65], suggests C5aR1 antagonism would be well tolerated and may slow cognitive decline in AD and other neurodegenerative diseases in which complement activation is excessive or not appropriately regulated. The gene discussed is VTN; the disease is neurodegenerative disease.