In addition, the evidence that (i) ALT may operate as a backup mechanism when telomerase is inhibited (Table 2 and Figure 2), (ii) ALT-positive cells are characterized by higher levels of telomeric DNA damage than telomerase-positive cells [9], and (iii) different factors involved in DNA damage repair are required to promote ALT activity in immortalized cell lines [60], which suggests that ALT may dictate the sensitivity of tumor cells not only to telomerase inhibitors but also to radiation [14] and DNA damaging agents [61]. Here, GPT is linked to neoplasm.