Telomeres are specialized structures located at the ends of chromosomes, playing a critical role in maintaining chromosomal integrity and stability. In normal cells, continuous telomere shortening with each cell division triggers DNA damage responses and initiates irreversible cellular senescence or apoptosis 5. Alternatively, chromosome instability and DNA damage‐induced genetic mutations due to shortened telomeres may result in neoplastic transformation 6, 7. It has been proposed that permanent proliferation of cancer cells depends on the maintenance of telomere length 8. To counteract telomere shortening, up to 90% of human cancers, including HCC, reactivate telomerase 9. Data have accumulated that tumor telomeres are shorter than normal tissues in the majority of human cancers 10, 11, 12, while longer telomeres in sarcomas and gliomas were also observed 13. Likewise, there are conflicting results regarding the impact of telomere length on cancer susceptibility and survival. For example, short telomeres predicted a poor prognosis in chronic lymphocytic leukemia and colorectal cancer, but a reduced death risk in esophageal cancer 14. Intrinsic biological features in each cancer demand that the clinical significance of telomere length needs cancer‐specific investigation. Although HCC has the second highest frequency of TERT promoter mutations among 31 cancer types 13, the clinical relevance of telomere attrition or elongation in HCC remains unknown.