The findings of our study, which investigated the relationship between NF-κB and MAPK-mediated proinflammatory microenvironment and amyloid accumulation in the kidneys of aged rats, revealed that aging-related low-grade inflammation induces histopathological changes in renal tissue but is not sufficient for amyloid accumulation in the primary target organs of systemic amyloidosis. Here, NFKB1 is linked to primary systemic amyloidosis.