Furthermore, the pathogenicity of this high affinity FcγR has been confirmed in animal studies; CD64- or FcRγ-chain deficient mice demonstrated decreased arthritic symptoms in the collagen-induced arthritis model, and treatment with a CD64-directed immunotoxin showed promising results in human CD64 transgenic rats suffering from joint inflammation [20–22]. This evidence concerns the gene FCGR2A and Arthritis.