Rolipram can induce expression of G1 CDK inhibitors p21Cip1 and p27Kip1 to inhibit growth, induce differentiation, and cause apoptosis.35 In turn, rolipram increased survival of mice bearing intracranial U87 glioma xenografts after treatment with temozolomide and IR, though not with IR only.36 In our study, pretreatment with rolipram enhanced accelerated senescence after irradiation suggesting that rolipram might also confer radiosensitization. Here, CDKN1A is linked to glioma.