To determine the role of MnSOD/FoxM1 axis modulation in isovitexin-associated inhibition or xenograft tumor growth in vivo, mice bearing HCSLC tumors were orally treated every 2 days with 200 μl of vehicle, 10 mg/kg isovitexin or 5 mg/kg thiostrepton (specific inhibitor of FOXM1), or intratumorally injected with adenovirus expressing MnSOD shRNA (once a week) or combination of isovitexin plus thiostrepton and adenovirus, respectively. This evidence concerns the gene FOXM1 and neoplasm.