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]. The gene discussed is TNF; the disease is rheumatoid arthritis.