In addition, the genetic deficiency of C5 has been shown to be one of a limited number of genetic differences associated with decreased amyloid deposition in DBA/2J mice versus C57Bl6 mice transgenic for the human APP gene (Ryman et al., 2008; Jackson et al., 2015), supporting a pathogenic role for C5a in the context of the AD brain in vivo. The gene discussed is C5AR1; the disease is Alzheimer disease.