NFKB1 and neoplasm: Concurrently, senescence-associated chronic inflammation fuels tumor progression through genomic destabilization: apolipoprotein B mRNA editing enzyme catalytic subunit 3B (APOBEC3B)-mediated cytosine deamination elevates mutation burden (2.5-fold higher in elderly patients) while NF-κB activation sustains pro-tumorigenic cytokine release (81).