Similarly, in breast cancer and glioblastomas, wild-type TP53 and the TP53-R273H gain-of-function mutant mediated the shuttling of BRCA1 from the nucleus to the cytosol, resulting in impaired HRR capacity and yielding a better response to PARPi after IR pretreatment [179]. This evidence concerns the gene TP53 and glioblastoma.