compared the effect of all-thiol form (at-HMGB1) and disulfide-HMGB1 (ds-HMGB1), two different redox states of HMGB1, on angiogenesis of colorectal carcinoma, and showed that at-HMGB1 stimulates ECs migration through interacting with RAGE, and ds-HMGB1 induced VEGF-A secretion by ECs through TLR4, both of which leaded to neovascularization in tumor microenvironment. This evidence concerns the gene HMGB1 and neoplasm.