Thus, both antagonists suppress tumor cell proliferation, reduce the size of tumor cells, downregulate cancer markers (e.g., mitogen-activated protein kinase 1 and Jun), upregulate tumor inhibitors (e.g., nexin and p53), block invasion and angiogenesis regulators (e.g., matrix metallopeptidase 1, angiopoietin 1, and S-100 calcium-binding protein), and favor autophagic and apoptotic mechanisms [109]. The gene discussed is JUN; the disease is cancer.