Elevated Cdc42 protein activity disrupts the immune system's capacity to eliminate senescent cells during aging, according to new research in Aging Cell. The study identifies a specific molecular mechanism where hyperactive Cdc42 interferes with immune cell function, allowing damaged senescent cells to accumulate rather than being properly cleared. This represents a significant advance in understanding why cellular waste removal becomes progressively inefficient with age. The Cdc42 pathway has been implicated in various aging processes, but this direct connection to senescent cell clearance provides new therapeutic targets. If confirmed in human studies, Cdc42 inhibition could enhance the body's natural ability to eliminate zombie cells that drive age-related inflammation and tissue dysfunction. The finding helps explain why senolytic drugs show promise—they may compensate for declining immune surveillance. However, Cdc42 also regulates essential cellular processes, so therapeutic modulation would require precise targeting to avoid disrupting normal cell division and migration. This mechanism could inform development of immune-boosting interventions that restore youthful cellular housekeeping rather than relying solely on pharmaceutical senolytics.