In p53-deficient glioblastoma tumors resistant to DNA-damaging agents, a crucial role has been found for CK2 also in PTEN localization: upon DNA damage, PTEN fails to accumulate in the nucleus, and is retained in the cytoplasm in its monomeric inactive state, due to its phosphorylation by CK2. This evidence concerns the gene TP53 and glioblastoma.