There is a complex feedback loop between senescence and inflammation. The observation that tubular cells isolated from CalpTG mice are not protected against senescence in vitro suggests that calpains promote first inflammation, which then leads to cellular senescence but we cannot rule out that in vivo, senescent cells participate in the vicious circle promoting inflammation. Cellular senescence is characterized by the secretion of proinflammatory cytokines (senescence associated secretory phenotype or SASP) including IL-1α, IL-1β, IL-6 or TNF-alpha. NF-κB regulates the majority of genes that comprise the SASP and NF-κB has been demonstrated to drive aging in brain and to be required to enforce many features of aging in a tissue specific manner28–30. We and other groups have previously evidenced that NF-κB nuclear translocation and activity was reduced in cells and tissues from CalpTG mice10, 22. Here, genome-wide gene expression profiling revealed that cytokines whose synthesis is regulated by NF-κB and that are involved in innate immune response were effectively down-regulated in old CalpTG mice in comparison to old controls.