Qu et al. (2015) found that in nude mice bearing human OS xenograft tumors, HMGB1 administration significantly increased angiogenesis in the tumor tissue. Recent research has also shown that angiogenesis was inhibited by SIRT1 activation, which downregulated VEGF transcription and inhibited angiogenesis induced by HMGB1 (Kim et al., 2014). Emodin, as a compound, deacetylates HMGB1 and attenuates angiogenesis induced by HMGB1 in OS by increasing SIRT1 expression and its deacetylation activity (Qu et al., 2015). This evidence concerns the gene HMGB1 and neoplasm.