TP53 and glioblastoma: In another in vivo study, rodent GBM models exhibiting ATRX and p53 loss demonstrated an impairment in non-homologous end joining (NHEJ) DNA repair, had decreased amounts of NHEJ-related proteins pDNA-PKcs, and were more responsive to double-stranded DNA-damaging therapy than controls with p53 loss alone but ATRX maintained (33).