AT1R signaling appears to be the main component of RAS involved in tumor growth by inducing vascular endothelial growth factor (VEGF) synthesis, angiogenesis, inflammation, upregulation of endothelial adhesion molecules and subsequent infiltration of inflammatory or cancer cells, trans-activation of multiple tyrosine kinases, and subsequent cell proliferation.6,8 AT1Rs8,9 and AT2Rs9 are over-expressed in cancer tissue and promote tumor progression.9 Both ARBs and ACEIs can reverse angiogenic and mitogenic effects of AT2 in cancer tissue.8 The gene discussed is VEGFA; the disease is cancer.