We established that: (1) Raf paradox signalling induced by dabrafenib in cardiac cells is limited; (2) dabrafenib inhibits ERK1/2 activity in isolated cardiac cells, in ex vivo perfused adult rat hearts and in a murine model of hypertension induced by angiotensin II (AngII); and (3), inhibition of Raf kinases with dabrafenib reduced cardiomyocyte hypertrophy, cardiac inflammation and cardiac fibrosis induced by AngII in both acute (7 d) and chronic (28 d) treatment conditions. This evidence concerns the gene AGT and Hypertension.