RS induce senescence through various mechanisms, including: (i) regulation of mammalian target complexes of rapamycin; (ii) production of pro-inflammatory interleukins, such as IL-1α, which stimulate factors like nuclear factor kappa-B (NF-κB); (iii) triggering chronic diseases such as cancer, Alzheimer’s disease, atherosclerosis, osteoarthritis, and emphysema; (iv) inhibiting forkhead box (FOXO) proteins involved in protection against OS; and (v) inhibiting the activity of sirtuin and SOD enzymes, thereby increasing OS and promoting a pro-inflammatory state [16,17]. Here, NFKB1 is linked to atherosclerosis.