Thus, quantification of RPA, γH2AX and H3K9me3 foci localized at telomeres in ALT or telomerase+ brain tumors suggests that the rescue of ALT by telomerase overexpression may be mediated by a reduction of telomeric DNA replication, with consequently reduced replication stress, and re-establishment of protective telomeric heterochromatin, which also leads to a reduction of TIFs. The gene discussed is GPT; the disease is brain neoplasm.