Radiation-induced ROS compromise cellular macromolecules, inducing apoptosis and senescence.[7] Endothelial senescence, particularly due to post-radiation DNA damage, fosters a pro-inflammatory and pro-thrombotic environment, catalyzing atherogenesis.[10,17] ROS activate the nuclear factor-kappa B (NF-kB) pathway, enhancing expression of thrombosis and inflammation markers.[11] Radiation-induced molecules (VCAM-1, ICAM-1, E-selectin) worsen endothelial dysfunction by attracting and activating immune cells, perpetuating inflammation. The gene discussed is NFKB1; the disease is endothelial dysfunction.