Treatment with the nuclear factor-kappa B (NF-κB) inhibitors, pyrrolidine dithiocarbamate and parthenolide, abrogated the stimulatory effect of poly(I:C) on the production of VEGF and IL-8 in RA FLS, which suggests that targeting the NF-κB signaling pathway may prevent the upregulation of pro-angiogenic molecules in RA FLS [11]. Here, NFKB1 is linked to rheumatoid arthritis.