For instance, CUL4A overexpression delayed the accumulation of p53 in response to DNA damage in mouse embryonic fibroblasts, which was dependent on MDM2.[12] Therefore, CUL4A could suppress DNA damage response and promotes cell survival in PC12 cells subjected to hypoxia and reoxygenation.[24] These cells survived from reduced repair proficiency might initiate carcinogenesis and contribute to tumor recurrence after chemotherapy and radiotherapy.[25] The latter hypothesis was also supported by our result that NPC patients with higher CUL4A expression had shorter PFS time. Here, MDM2 is linked to neoplasm.