Genetic alterations that create additional ETS‐binding sites in the vicinity of native sites are a known mechanism of aberrant TERT activation in cancer.19 In fact, Bell et al showed that c.‐124C > T and c.‐146C > T cooperate with native ETS sites, especially with ETS‐195 and ETS‐200, to recruit GA‐binding protein (GABP) transcription factor and to directly initiate the upregulation of TERT expression in glioblastoma.19 They also showed that, in addition to point mutation creating de novo ETS sites, a duplication event of 41‐bp generates one de novo ETS motif in one tumor. Here, TERT is linked to cancer.