Indeed, Fcγ receptor IIa (FcγRIIa; cluster of differentiation [CD]32a) and FcγRIIIa (CD16) expression is increased in monocytes/macrophages from patients with RA, and these cells have been shown to produce higher levels of TNF-α and MMPs than those from healthy controls [11]. This evidence concerns the gene FCGR3A and rheumatoid arthritis.