This finding is distinct from that observed in cancer cells, where robust apoptotic signals are induced by the activation of p53 via MDM2 degradation.[18] The reported p53 dynamics could explain these distinct effects depending on the cellular context: sustained p53 levels typically lead to senescence and apoptosis, whereas oscillatory p53 activity selectively activates genes involved in DNA damage repair.[26] This suggests that p53 dynamics may have cell type‐specific effects, influencing distinct cellular responses to MDM2 degradation. Here, MDM2 is linked to cancer.