These results showed that compared with that of RA-FLSs stimulated by IL-34 alone, the proliferation of RA-FLSs stimulated with IL-34 and PB was significantly inhibited, the rate of apoptosis was significantly increased, and the mRNA levels and protein levels of proinflammatory cytokines (IL-6 and TNF-α) and angiogenic factors (VEGF and HIF-1α) decreased significantly. The gene discussed is TNF; the disease is rheumatoid arthritis.