Taken together, these observations suggest that the reduction of rad21a levels leads to a decrease of DSB repair efficiency, and, at the same time, relieves the transcriptional repression on tert in previous ALT+ tumors; thus, allowing telomere maintenance of tumor proliferating cells through other mechanisms, either through a partly restored telomerase dependent mechanisms, or through telomerase- and ALT-independent mechanisms [35], or both. This evidence concerns the gene GPT and neoplasm.