These effects, in fact, are mediated by the inhibition of isoprenoid intermediates, which are responsible for post-translational modifications of these small GTP-binding proteins and involve the following: (i) the decrease of oxidative stress through the reduction of ROS levels; (ii) the reduction of inflammation by preventing the dislocation of IkB from NF-kB, resulting in its inactivation; and (iii) the reduction of cardiac hypertrophy risk [15,16]. The gene discussed is NFKB1; the disease is cardiac hypertrophy.