Specifically, by recreating the risk conditions for the development of cardiac hypertrophy associated with atherosclerosis, we first followed the changes that occur at the functional, structural, and molecular level in the left ventricle, mediated by Ang II and TGF-β1 via SMAD2/3, and NF-kB signaling molecules. This evidence concerns the gene NFKB1 and cardiac hypertrophy.