Limitless replicative potential is considered a hallmark of cancer, which is achieved by an inappropriate reactivation of the essential enzyme telomerase [1, 2]. Telomerase maintains telomere integrity by adding the six-nucleotide repeat sequence, 5′-TTAGGG, to the ends of the chromosomes using its internal template RNA component (TERC) and reverse transcriptase protein component (TERT), thus counteracting the telomere shortening that naturally occurs during DNA replication [3–6]. Telomerase is not expressed in most adult somatic cells and the telomeres are therefore progressively shortened with each round of replication, which ultimately leads to replicative senescence and thus a finite replicative potential. In contrast, stem cells and cancer cells have high telomerase activity. In fact, TERT has been shown to be overexpressed in almost 90% of all human malignancies, but although there is evidence that mutations in the TERT promoter lead to enhanced TERT expression, the mechanisms by which telomerase is reactivated is still poorly understood [7–11].