Noteworthy, the combined therapy with LCL-SIM and LCL-DMXAA strongly reduced (by 50–81%) the intratumor production of bFGF, IL-1 α/β, IL-6, TNFα, leptin and of eotaxin, which allow cancer cells to escape VEGF-targeted therapies, promoting tumor growth and metastasis47,48. The gene discussed is FGF2; the disease is neoplasm.