In our previous study, we demonstrated that HSV-HMGB1 (lacking both copies of ICP34.5 and harboring the HMGB1 sequence in the TK locus) could kill colorectal cancer cells more efficiently than the parental virus during hypoxia or normoxia, except for the HT29 cell line, in which HSV-HMGB1 enhanced the viability of cells under hypoxic conditions. Here, HMGB1 is linked to colorectal cancer.