Encouragingly, thalidomide has been shown to induce monocyte apoptosis through endogenous mitochondrial pathways by promoting the release of Cyt c, activating caspase-3, caspase-9, and NF-κB; and inhibiting Akt-1 activity thereby facilitating the treatment of RA (81). This evidence concerns the gene NFKB1 and rheumatoid arthritis.