Cell‐cycle arrest without undergoing cell death process is a hallmark of cellular senescence, which usually contributes to aging‐related diseases.[16] As expected, the expressions of senescence markers, including senescence‐associated β‐galactosidase activity (SAβG), phosphorylated histone H2AX (γ‐H2AX), p53, and p16, were significantly increased in the aortas and fibrous cap VSMCs of CKD/ApoE−/− mice (Figure 2D,F; Figure S2C–H, Supporting Information). The gene discussed is TP53; the disease is glycogen storage disease VI.