More specifically, several in vitro studies highlighted the capability of CTLA4-Ig treatment to reduce the gene expression and release of pro-inflammatory cytokines IL-6, IL-1β, and TNFα directly interacting with CD86 on the surface membrane of APCs, primarily synovial macrophages and monocyte-derived macrophages isolated from RA patients (104, 105). The gene discussed is TNF; the disease is rheumatoid arthritis.