In rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs), bufalin treatment has a dose-dependent inhibitory effect on IL-1β-induced proliferation by downregulating mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB), and suppressing apoptosis through a mitochondrial-dependent pathway (Chang et al., 2014). Here, NFKB1 is linked to rheumatoid arthritis.