The current study offer an evidence that MG and GA may be the main BACs of BHGZD for their strong binding affinities with components of predicted targeted signal axis, high exposed quantity in vivo, and prominent effects in restricting disease severity by reducing synovial inflammation and restricting excessive synovial vascularization during RA progression, the mechanisms of which may be associated with its regulatory effects on the VEGFA/VEGFR2/SRC/PI3K/AKT signal axis. The gene discussed is KDR; the disease is rheumatoid arthritis.