In vitro studies performed in cardiac fibroblasts isolated from Fbln2-/- mice showed that FBLN2 plays an essential role in angiotensin II-induced TGF-β signaling pathway, while studies performed in a murine model of cardiac hypertrophy demonstrated that Fbln2-/- mice show attenuated development of cardiac hypertrophy induced by chronic infusion of subpressor and pressor doses of angiotensin II [36]. The gene discussed is AGT; the disease is cardiac hypertrophy.