Using direct and indirect co-cultivation, Donlin et al. demonstrated that human RA synovial fibroblasts suppress the TNF-α-induced IFN-γ signature in macrophages under both conditions, indicating that no cell contact is required, but rather soluble fibroblast products inhibit the IFN-γ signature of macrophages [86]. The gene discussed is IFNG; the disease is rheumatoid arthritis.