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. The gene discussed is NFKB1; the disease is atherosclerosis.