The unique signature of the liver microenvironment, characterized by a chronic inflammatory state and dysregulated immune response, was associated with the biological behavior of HCC 15. Within the HCC microenvironment, cancer‐associated fibroblasts (CAFs) and tumor‐infiltrating lymphocytes (TILs) are of paramount importance. Experimental and clinical evidence demonstrated that interactions between CAFs or TILs and tumor cells could promote HCC progression and metastasis through various mechanisms 16, 17. A recent study in prostate cancer suggested that investigation of telomere length in cancer‐associated stromal cells is feasible and is significant for predicting cancer behavior 18. Large‐scale prospective studies suggested that telomere attrition in peripheral blood leukocytes correlated not only to poor prognosis of a group of human cancers 19, 20 but also with increased mortality in the general population 21. Thus, it is rational to speculate that telomere attrition or elongation in CAFs or TILs would harbor significant clinical value in HCC.