AGT and cancer: The selective blockade of AT1R will lead to an indirect stimulation of angiotensin type 2 receptor (AT2R)[3] and increase the metabolism of Ang II into Angiotensin 1 to 7, both inducing vasodilation, natriuresis, and endothelial antiproliferative actions.[4] Both molecular and cellular evidence were found indicating that the expression and actions of the RAAS influence malignancy and also predict that RAAS inhibitors can play a role in cancer pathogenesis.[7]