Liu et al demonstrated that the neuronal C-reactive protein/FcγRI positive feedback pro-inflammatory signaling pathway plays a significant role in nerve injury-induced neuropathic pain.[32] Additionally, Jiang et al and Lacagnina et al further validated the involvement of the B cell–IgG–FcγR axis in the pathogenesis of neuropathic pain.[33,34] In the musculoskeletal system, FcγRs are implicated in autoimmune conditions such as rheumatoid arthritis. This evidence concerns the gene FCGR2A and rheumatoid arthritis.