Previous data in mouse models of atherosclerosis (ApoE−/− and/or LDLR−/− background) show the involvement of the following complement components in the pathogenesis; C3, C1q, CD59, CD55 also known as decay accelerating factor (DAF), and MBL (reviewed in [6]) with an emerging role for C3adesArg in particular. This evidence concerns the gene C3 and atherosclerosis.