In the CAIA mouse model of rheumatoid arthritis, pharmacological antagonism of the C5a receptor did not block the development of pain-related behavior in response to CII autoantibodies, and complement 5 knockout (C5−/−) mice likewise develop pain-related behavior like wild-type mice.12 These results indicate, at least for the CAIA model, that pain hypersensitivity develops independently from C5. Here, C5 is linked to rheumatoid arthritis.