Nevertheless, as a therapeutic agent of RA, SIN could inhibit the development and progression of CIA in rats [28], might inhibit bFGF-induced angiogenesis in vitro and in vivo [29], could induce the apoptosis of macrophages through activation of the ERK pathway, and inhibit proliferation and induce apoptosis via activation of caspase 3 of CD4+ T cells [30]. Here, FGF2 is linked to rheumatoid arthritis.