Of note is that the functional mechanism of ATO is manifold—for example, it has been shown that ATO can induce apoptosis by increasing the intracellular reactive oxygen species concentrations and the activation of caspase-dependent apoptosis pathways, inhibit tumor-induced angiogenesis by downregulating VEGF, and induce cell cycle arrest in the G2/M phase by regulating cyclinB and Bcl-2 (24). This evidence concerns the gene VEGFA and neoplasm.