In the angiotensin II (Ang II) infusion model, absence of fibulin-2 inhibits Ang II-induced myocardial hypertrophy and fibrosis in vivo with suppression of TGF-β signaling, indicating a critical role of fibulin-2 in Ang II-induced TGF-β activation and its downstream signaling [133,134]. This evidence concerns the gene FBLN2 and cardiac hypertrophy.