CDKN2A and neoplasm: While cellular senescence functions as a tumor-suppressive mechanism by preventing the proliferation of damaged cells [18, 20], accumulating evidence indicates that IR-induced senescence, facilitated by high expression of p16, not only halts cell proliferation but also drives the SASP, thereby influencing tissue homeostasis, promoting inflammation, and tumorigenesis via releasing SASP factors consisting of various pro-inflammatory cytokines, growth factors, and proteases [21–24].