Components of SASP can induce senescence of nearby non‐senescent cells in a paracrine manner, thereby increasing the overall number of senescent cells.[28] In addition, abnormal mitochondria produce excessive ROS, which further activates the p38 MAPK pathway and enhances SASP secretion.[29] CD4+ T cell senescence can induce chronic systemic inflammation and aggravate the systemic senescence phenotype,[30] indicating that SASP may be both a result and cause of aging. This evidence concerns the gene CD4 and inflammation.