At secondary-structure loci, the G4-stabilising ligand telomestatin elevates RPA32-Ser33 phosphorylation in human glioma stem cells, accompanied by TRF2 (Telomeric repeat-binding factor 2) loss from telomeres and CHK1 activation; pSer33 foci form in a replication/transcription-dependent manner, while matched non-stem glioma cells show pS33 without robust checkpoint engagement [243]. Here, CHEK1 is linked to central nervous system cancer.