Telomerase reactivation, either via the chromosome end‐replicating enzyme telomerase reverse transcriptase (TERT) or alternative lengthening of telomeres, is detected in up to 80% of malignant tumours.1, 2 Somatic mutations in the TERT promoter were first identified in melanoma3, 4 and have been observed at high frequency in multiple cancer types, including those of the thyroid, central nervous system and bladder.5, 6, 7 These mutations occur at two hotspots, chr5:1,295,228C>T (‘C228T’) and chr5:1,295,250C>T (‘C250T’), located, respectively, −124 and −146 bp upstream from the ATG start site. This evidence concerns the gene TERT and cancer.