In breast cancer models, garcinol counteracts estrogen-driven proliferation by lowering acetyl-p65 levels and suppressing cyclin D1, Bcl-2, and Bcl-xL expression, while simultaneously activating caspases and other pro-apoptotic mediators—effects largely attributed to the inhibition of NF-κB signaling [38,39,40,41,42]. Here, NFKB1 is linked to breast cancer.