Although a conclusive evidence of ACRH, QRF, and BQ acting on in vitro signaling of RA angiogenesis is yet to be defined, however, their inhibition against the in vitro HFLS-RA cellular functions observed in this study is hypothesized via suppression on the IL-1β-mediated activation of signaling pathways associated with the cell proliferation, invasion, and survival of HFLS-RA. This evidence concerns the gene IL1B and rheumatoid arthritis.