Previous publications demonstrated that Trip13 loss‐of‐function reduces tumor growth in head and neck cancer and colon cancer, as well as more recently in HCC.[16] The oncogenic effects of Trip13 have mainly been attributed to an enhanced capacity for DNA damage repair, particularly through DNA–dependent protein kinase c (DNA–PKc)‐dependent nonhomologous end joining, thereby contributing to genomic instability.[16] In fact, we were able to prevent Trip13‐KD‐induced cell death by interfering with the DNA damage response through inactivation of the ATM/ATR pathway. This evidence concerns the gene ATR and hepatocellular carcinoma.