Answering these questions is a prerequisite for testing the hypothesis that clearance of senescent macrophages can prolong lifespan/healthspan in animal models. So far, genetic engineering and pharmacological approaches aimed to remove SCs from the organism have shown variable success in restraining inflammation in different organs, including, kidney and fat, thus increasing mice lifespan and/or healthspan. ABT263, a senolytic agent targeting both antiapoptotic proteins, BCL-xL and BCL-2, has recently been shown to induce apoptosis in SCs, rejuvenating aged bone marrow hematopoietic stem cells [5]. Interestingly clodronate treatment, which kills phagocytic cells, has been reported to induce a drastic reduction of ageassociated inflammatory responses to systemic immunostimulation in aged mice [6]. Recent data on mice demonstrating that foamy macrophages with senescence markers accumulate in the sub-endothelial space, driving atherosclerotic process by increasing expression of inflammatory cytokines, chemokines, and metalloproteinases, strongly support the involvement of macroph-aging in the development of ARDs [7]. If the intriguing hypothesis that the accumulation of senescent macrophages contributes to accelerate the aging processes in humans is demonstrated, work on senolytics will need to be integrated by research into senescent macrophage-lytics.