When the chemotherapeutic effects of oral silibinin on the growth and progression of established, urethane-induced, lung adenocarcinomas in A/J mice were studied, its strong ability to suppress both tumor number and size correlated with a reduced antiangiogenic activity mediated by decreased cytokine production in tumor-associated macrophages and suppression of NFκB and STAT3 activation in lung cancer cells [36]. This evidence concerns the gene STAT3 and neoplasm.