As far as the possible pathogenetic mechanisms are concerned, while overexpression of farnesyl pyrophosphate synthase (FPPS) results in cardiac hypertrophy in mice, the targeted inhibition of FPPS by NCBSPs results in an attenuation of cardiac hypertrophy through inhibition of the mevalonate pathway leading to prevention of ischemia-induced myocardial remodeling [43]. The gene discussed is FDPS; the disease is cardiac hypertrophy.