More efforts have been focused on the telomerase inhibitors due to high incidence (80–90%) of telomerase activation as compared to ALT (10–20%), which is most prevalent in tumours such as astrocytomas, glioblastomas, osteosarcomas, fibrous histiocytomas and liposarcomas.11, 40 Recently, an ATR inhibitor, VE-821 was shown to cause stronger DNA damage to ALT cancer cells.41In vitro studies have demonstrated that telomerase and ALT mechanism can coexist within individual cancer cells.9 Inhibition of TEP could activate ALT or vice versa42, 43 raising the need for dual action inhibitors. This evidence concerns the gene ATR and neoplasm.